EMSS2017: Dyspnoea Course Materialemss17.sats-kbh.dk/wp-content/uploads/2017/07/EMSS17-Dyspnoe… · Dyspnoea 2 emss17.sats-kbh.dk observe whether a patient can finish a sentence

Dyspnoea

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EMSS2017: Dyspnoea Course Material

During this workshop, you will learn about the definition, basic pathophysiology, a selection of causes and

Relevant acute diagnostic procedures of acute dyspnoea, as well as treatment for the same selection of

causes.

This written material will serve as an introduction, and will present and describe the underlying causes of

acute dyspnoea that will be focused upon on the course, as well provide supplementary information about

differential diagnostics.

Definition and the basics Dyspnoea is defined as the subjective experience that one’s breathing is inadequate, and is called shortness

of breath in laymen’s terms. The experience is uncomfortable, and pathologic, as it is also defined by not

being proportional to the patient’s current level of exertion. Dyspnoea is often accompanied by a rise in

respiratory rate, called tachypnoea (if it exceeds 20 breaths per minute), and/or an increase in deepness of

breath, called hyperpnoea. These may, separately or in conjunction, result in an increase in ventilation,

called hyperventilation. If alveolar ventilation is lowered, or gas exchange is impaired, patients can have

lowered SAT (below 92% if >40 years or below 95% if <40 years) or hypoxemia (PaO2 below 9,6 kPa). Some

will have hypercapnia (PaCO2 above 6,0 kPa), but some patients might have hypocapnia (PaCO2below 4,6

kPa) because of alveolar hyperventilation.

The New York heart association (NYHA) has created a useful, four-tiered scale of heart failure symptoms,

including dyspnoea, mainly focusing on the degree of exertion required to provoke the symptom:

Grade I: No limitation of physical activity. Ordinary activity does not cause dyspnoea.

Grade II: Slight limitation of physical activity. Comfortable at rest. Ordinary physical activity results in,

dyspnoea.

Grade III: Marked limitation of physical activity. Comfortable at rest. Less than ordinary activity causes

dyspnoea.

Grade IV: Unable to carry on any physical activity without discomfort. If any physical activity is undertaken,

discomfort increases. Dyspnoea is present even at rest.

The full original scale also includes other elements, reflecting its focus on cardiac disease, but is presented

here in a simplified form, including only assessment of dyspnoea. The scale in this form is useful in

describing acute changes, as well as chronic dyspnoea.

As with any symptom, it is important to make several distinctions when taking patient history. How acutely

has the dyspnoea progressed?

A debut within 48 hours of first presentation is often called acute, and presents different diagnostic

considerations than with slower progressing types of dyspnoea. It also important to note the actual debut

of the symptom; was it sudden or creeping? Was it related to other symptoms? (E.g. cardiac or pleural

chest pains) Is there anything that worsens or relieves the symptom? (E.g. lying down worsens cardiac

dyspnoea because of an increased pre-load and strain on the heart). Sometimes it can also be useful to

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observe whether a patient can finish a sentence without having to stop and catch their breath. An inability

to do so is called speech dyspnoea.

The Dyspnoea Workshop on EMSS2017 will focus on five principal pathologies behind acute dyspnoea, of

either cardiac or pulmonary origin. These are presented in the following sections, followed by some

honourable mentions and additional diagnostic considerations that will not be the focus of the workshop.

Finally, a full list of abbreviations used is provided at the end of the document. Please note that doses and

specific medicine is sometimes mentioned in this document for the sake of completeness, but we

encourage you to focus on principles of treatment, rather than details, when preparing for the workshop.

Exacerbation of COPD

Definition: An exacerbation of COPD is an incident with deterioration of existing respiratory symptoms, requiring

additional treatment beyond the patient’s usual medication. It is usually classified into the following

groups, based on severity:

Mild: a state that can be treated with an addition of/increase in short-term bronchodilators

Moderate: a state that requires treatment with antibiotics and/or systemic corticosteroid

Severe: a state that requires hospital admission or emergency department visit

Pathophysiology, aetiology and pathogenesis: Exacerbation is most often caused by bacterial or viral infection, but other possible causes can be air

particle pollution, smoking, heart disease, anxiety/panic attacks and climatic changes. For one third of

patients, an underlying cause is never identified.

Patient history and symptoms: Risk factors for COPD in general are smoking, age, low socioeconomic status as well as general and work-

related air pollution. A rare few cases are caused by a genetic alfa1-anti trypsin deficit, which is often known

to be in the patient’s family.

The patient will often have a known history of COPD, but an exacerbation can be their first contact for their

respiratory symptoms. Comorbidity with heart disease and lifestyle diseases is common.

Symptoms include an increase in dyspnoea, an increase in sputum and coughing, with an acute to sub-

acute debut.

Presentation upon clinical examination: The patient will present with varying degrees of respiratory distress, according to the severity of their

underlying COPD and the current state of exacerbation. Severely affected patients will be unrestful, anxious

and will be visibly reliant on accessory muscles of respiration. SAT will often be below 90% without

supplemental oxygen, and the respiratory rate elevated above 20/min (both of which can be a chronic

condition for COPD patients), and the patient might have cyanosis.

Chronic COPD patients might have a classic barrel-chest, as an indication of an overinflated thorax

(difficulty with performing a full expiration).

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Upon pulmonary auscultation, one can hear a prolonged expiratory period, with rhonchi and coarse basal

crepitation. Cardiac auscultation will often sound normal. Emphysema can dampen both cardiac and

respiratory sounds.

Relevant acute diagnostic procedures: Arterial blood gas analysis can help elucidate any hypercapnia or hypoxemia, and help reaching

therapeutic targets for these parameters.

Principal blood tests are hgb, leukocytes, thrombocytes, sodium, potassium, kidney markers, liver markers

and CRP

Sputum should be sent to cultivation and resistance determination, so antibiotic treatment can be targeted

beyond an empirical approach.

ECG should be recorded to elucidate heart failure due to ischemia or arrhythmia, contributing to the

current exacerbation, or as a differential diagnosis.

CXR can be useful to visualise infection, current level of emphysema, cardiomegaly and pleural effusion.

Diagnosis: Diagnosis is reliant on the abovementioned examinations, and a history of COPD or newly discovered COPD

with FEV1/FVC < 0,7.

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Treatment: Treatment is dependent upon severity of the state of exacerbation. Mild and some moderate states can

often be treated by general practitioners, without hospital admission. Increasing steps are taken with

increasing severity of exacerbation, but it is important to also consider the severity of the underlying COPD,

and the stability of the patient’s respiratory function, when deciding treatment and possible admission.

Pathology Treatment Target patients Worsening of dyspnoea • Inhaled SABA (such as

salbutamol, fenoterol or terbutaline), with addition of SAMA (such as ipratropium) if monotherapy is insufficient

• Mild, moderate and severe exacerbation

Increase in pulmonary inflammation

• Systemic steroid, such as prednisolone 37,5 mg x 1 orally for 5 days

• Mild, moderate and severe exacerbation

• Is, by definition, not strictly needed to treat mild exacerbation, but speeds up bettering of symptoms

Hypoxemia, with SAT < 88 % or/and PaO2 ≤ 8,0 kPa

• Supplemental oxygen therapy • All Patients requiring admission

Respiratory dysfunction • An I.V. methyl xanthine • Moderate or severe exacerbation, in which respiratory symptoms are resistant to treatment

• Confer with senior colleague • Should not delay NIV if criteria

for this is met

Pulmonary infection • If the patient is poor general condition, consider empirical I.V. antibiotics

• If a patient is in good general condition, consider empirical oral antibiotics

• Always keep up to date with the suggested empirical treatment at your specific location of practice

• Mild, Moderate and severe exacerbation with a least one of: Increase in purulent sputum and increase in dyspnoea OR Substantial increase in infection-related parameters (CRP >50 mg/L), OR if the Patient receives NIV or invasive ventilation

Acute respiratory insufficiency that persists despite 1 hour of standard treatment and the

following:

• Blood pH < 7,35 and PaCO2 > 6 kPa

• And one of: Worsening in dyspnoea OR Respiratory rate > 25 OR PaO2 < 7 kPa

without supplemental oxygen

• NIV • Contact pulmonary or intensive care unit (or others responsible for NIV) to arrange treatment

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Status Asthmaticus

Definition: Status asthmaticus is an acute condition in asthma patients with increasing respiratory difficulty,

progressing over hours to days, with an accompanying reduction in pulmonary function (PEF and/or FEV1).

Pathophysiology, aetiology and pathogenesis: Status asthmaticus can develop for many reasons, such as poor compliance with treatment (especially

steroid inhalations), infections, cold or warm temperatures or allergic reactions. Some patients are

sensitive to Acetyl Salicylic acid and NSAIDs, which can trigger SA and all asthma patients are sensitive to β-

adrenal inhibitors, especially nonspecific agents.

Patient history and symptoms: Patients are typically young and otherwise healthy. Their asthma may be known, but a status asthmaticus

can also be the debut of the disease.

Cardinal symptoms are dyspnoea, tightening of the chest and coughing, developed acutely to sub -acutely.

Presentation upon clinical examination: Patients will appear with a varying degree of respiratory distress. The following table shows different

degrees of severity, along with symptoms and objective signs.

Moderate acute asthma Increasing symptoms PEF >50–75% best or predicted No features of acute severe asthma

Acute severe asthma Any one of:

• PEF 33–50% best or predicted - respiratory rate ≥25/min

• heart rate ≥110/min • inability to complete sentences in one breath – speech

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Life-threatening asthma Any one of the following in a patient with severe asthma: Clinical signs Measurements

Altered conscious level PEF <33% best or predicted

Exhaustion SAT <92% Arrhythmia PaO2 <8kPa

Hypotension “normal” PaCO2 (4,6-6,0 kPa) Cyanosis

Silent chest (upon pulmonary auscultation)

Poor respiratory effort

Near-fatal asthma Raised PaCO2 and/or requiring mechanical ventilation with raised inflation pressures

Relevant acute diagnostic procedures: Arterial blood gas analysis is central to assess severity of the status asthmaticus as the typically young

patients can appear in much better condition than they are. Since hypoxemia is a sign of severe, life -

threatening asthma, and hypercapnia is a sign that is closely followed by complete type II (hypercapnic)

respiratory failure, blood gas analysis should be repeated, and followed closely.

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Relevant blood tests are infectious parameters, such as CRP and leukocytes, in order to rule out infection

as a catalyst for the status asthmaticus.

CXR can be useful to explore differential diagnoses, e.g. pneumothorax.

Diagnosis: Diagnostics are aided by a patient’s history of asthma, reversibility of their condition with bronchodilators,

as well as the table above, under Presentation upon clinical exam.

Treatment: Treatment Target patients

Initial treatment • Liberally administered supplemental oxygen therapy as needed

• Inhalation with a SABA (such as salbutamol, fenoterol or terbutalin) in combination with a SAMA (such as ipratropium)

• Systemic corticosteroid injection, e.g. methylprednisolone 80 mg. I.V: or prednisolone 30-50 mg. x1 orally

• Magnesium sulphate can be considered in conference with senior colleague

All acute status asthmaticus patients

Substantial worsening of symptoms

• Consider need for intensive therapy and contact intensive care unit

Patients with • Dropping PEF

• Persistent hypoxemia

• Hypercapnia • Respiratory acidosis

• Respiratory exhaustion

• Changes in cognition • Respiratory stop

• Criteria for life-threatening or near-fatal asthma (se previous table)

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Pulmonary Embolism

Definition: Complete or partial closure of a pulmonary artery.

Pathophysiology, aetiology and pathogenesis: PE is most often caused by an embolus from DVT in the deep veins of the legs and/or pelvis, and the

collective term is venous thromboembolism. Changes in coagulation/fibrinolysis-balance, the venous

endothelium and the mechanics of blood flow in the deep veins result in DVT.

The PE results in varying degrees of impaired gas transport and vascular obstruction, which leads to

respiratory impairment and rising pressure in pulmonary arteries, often with RVHF.

Patient history and symptoms: Risk factors include recent surgery, immobilization, pregnancy, overweight, age, cancer, COPD, chronic

heart failure, previous DVT or PE, thrombophilia, oral contraceptives and postmenopausal hormone

treatment.

Many cases of PE are overlooked, as the symptoms can be both diffuse and unspecific. Many patients will

experience acute dyspnoea, respiratory chest pain, coughing, anxiety and unrest. Some w ill also

experience haemoptysis, and some can experience syncope(s).

Presentation upon clinical examination: Patients will have varying degrees of respiratory distress, reflecting the severity of their specific PE. Most

will appear anxious, unrestful and prefer sitting up. Pulmonary auscultation can appear normal,

uncharacteristic or there can be audible pleural friction. SAT will often be below reference intervals and

pulse and respiratory rate will often be above.

In some cases, the PE is severe enough to cause circulatory collapse because of vascular blockage in the

pulmonary circulation, restricting blood flow to the left ventricle, and causing right ventricle congestion.

This will result in severe and hyper acute symptoms of circulatory failure, along with severe dyspnoea,

cyanosis.

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Clinical assessment of a possible PE patient can be difficult. One can use Well’s score, to help assess the

likelihood of PE, based on a clinical examination:

Well’s Score Likelihood of PE

Point total

Variable Points awarded

Low 0-1

Risk factors:

• Previous DVT or PE

• Recent surgery or immobilization • Cancer

1,5 1,5 1

Intermediary 2-6

Symptoms:

• Haemoptysis

1

High ≥7

Clinical signs:

• Pulse > 100/min • Clinical signs of DVT

1,5 3

Clinical assessment

• Alternative diagnosis considered less probable than PE

3

Relevant acute diagnostic procedures D-Dimer in blood is a product of fibrin degradation, and is imperative for elucidation of a possible PE. The

blood test can often give a false positive, but is especially useful for ruling out PE, when clinical examination

with Well’s score assesses a low to intermediary risk of PE.

ECG will show characteristic findings in the form of sinus tachycardia and/or right sided heart strain with

negative T-waves in V1-V4, QR-pattern in V1, SI and QIII-TIII pattern, as well as incomplete or complete

right bundle branch block.

Ultrasound of the lower extremities can help to indicate PE, if it shows signs of DVT.

Cardiac biomarkers in the form of troponins and NTproBNP are of prognostic value in PE patients, and are

used to determine risk of 30-days-mortality as seen below.

Diagnosis: Diagnosis is done using the Well’s score and mentioned diagnostic procedures in conjunction. A high clinical

risk of PE often overrules examination findings, in that they are not always enough to rule out PE.

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Treatment: Treatment is determined by risk stratification, based in part on the sPESI score:

Simplified PESI score Parameter Points

Age 1 if age is > 80 years

cancer 1 Chronic Heart Failure OR 1

Chronic pulmonary disease Pulse ≥100/min 1

SAT 1 Systolic BP < 110 mmHg 1

The sPesi score is then used to provide a final estimate of 30-days mortality

30-days mortality risk Parameter or score

Shock or hypotension

sPESI ≥1 Signs of RVHF on TTE

Cardiac biomarkers (TnT or NTproBNP)

High + (+)* + (+)*

Intermediary Intermediary-high

- + Both positive

Intermediary-Low

- + 0-1 positive

Low - - Examinations optional, if taken both need to be negative

* : if patient is in shock, both sPESI score and laboratory test are not pertinent.

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Based on the risk stratification above, treatment is as follows:

Patients Treatment

All Acute treatment upon strong suspicion of LE:

• Supplemental oxygen therapy

Low risk • NOAC or LMWH/warfarin, possibly in ambulant care

Intermediary-low risk • NOAC (rivaroxaban or apixaban) alone OR warfarin with a supplement of LMWH for 5 days or until INR is in therapeutic range OR LMWH for 5 days or until INR is in therapeutic range, followed by dabigatran

Intermediary-High risk • Close clinical observation

• UFH. Bolus of 80 IU/kg IV, followed by 18 IU/kg/hour. Maintenance dose is adjusted according to aPTT, which is sought to be lengthened by a factor of 1,5-2,5 of the initial value. APTT is controlled 4-6 hours after treatment initiation, and every 6th hour thereafter OR

• LMWH by weight (reduction of dose if GFR<20 ml/min). For example: Dalteparin 200 IU/kg x1 subcutaneously

• If patient condition worsens, consider conferring with surgeon in order to plan embolectomy or perform thrombolysis

• If patient condition betters, consider change to treatment as for intermediary-low risk.

High Risk • Circulatory stabilization

• UFH as described under intermediary-high risk

• Contact senior colleague to arrange Thrombolysis or surgical embolectomy

• After stabilization: consider interchanging UFH treatment with LMWH by weight combined with warfarin

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Acute Coronary Syndrome

Definition: ACS covers three different conditions of myocardial ischemia, of which two are myocardial infarctions:

STEMI is, as the name implies, a case of AMI characterized by an elevation of the ST-segment of an ECG.

Non-STEMI is, as the name implies, a case of AMI characterized by the absence of an elevation of the ST-

segment of an ECG, with or without other signs of ischemia.

UAP is characterized by cardiac chest pains (described below) at rest or minimal exertion or a worsening in

stable, chronic AP. There can be only transient or exertionally related ST-changes in an ECG, and this

condition is not a myocardial infarction. UAP can, however, progress to an AMI, and is therefore put in the

same category when it comes to diagnostics and treatment.

Pathophysiology, aetiology and pathogenesis: The underlying pathology is most often occlusion of cardiac arteries by atherosclerosis, with or without

plaque rupture and thrombus formation, resulting in pain and/or myocardial necrosis. It is possible to

detect a thrombus in nearly all cases of STEMI, whereas this is possible in fewer cases for UAP and Non -

STEMI.

Patient history and symptoms: Risk factors include age, male sex, familial disposition, lipidaemia, hypertension, smoking, severe mental

stress, physical inactivity, overweight and diabetes.

The cardinal symptom of ACS is acute chest pain, characterized a pressure, heaviness, tightness or

squeezing behind the sternum and across the chest, often radiating to the neck area, jaw, shoulder and

arm. It can also be experienced in the back and epigastrium. The pain is not typically related to movement,

such as breathing.

Other common symptoms are dyspnoea, malaise, nausea, vomiting, sweatiness and syncopes.

Presentation upon clinical examination: The patient can appear confused; have impaired consciousness and mental unrest. The patient will often

appear pained. BP and pulse can often be unremarkable, or can be affected in more severe cases, with

symptoms of cardiogenic shock, pulmonary oedema or even cardiac arrest. Respiratory rate is often

elevated.

Cardiac auscultation is most often unremarkable, but a murmur could be a sign of ischemic mitral

insufficiency. Pulmonary auscultation is most often unremarkable, but crepitation can be a sign of

ischemically induced cardiogenic pulmonary oedema.

Relevant acute diagnostic procedures: ECG is essential for a diagnosis, as it identifies important electro myocardial signs of ischemia. It is taken

prehospitally, upon admission and in short intervals until diagnostic clarification is sufficient, eg. Every 15

minutes.

Biomarkers for myocardial necrosis in blood are obligatory, in the form of troponin T/I and creatine kinase-

MB, both upon admission and after 3 hours. These can be repeated if a suspicion of ACS remains.

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Other relevant blood tests: haemoglobin, thrombocytes, INR, CRP, sodium, potassium, creatinine, BS,

HgbA1C, total-cholesterol, HDL- and LDL-cholesterol and triglycerides.

Echocardiography is performed acutely, and a cardiologist should be contacted, if the patient is

hemodynamically unstable, if there are audible murmurs or if there is uncertainty regarding diagnosis or

possible complications.

Diagnosis: AMI is diagnosed by:

1. A rise and/or fall in myocardial biomarkers

And

2. Indication of myocardial ischemia by at least one of the following:

a. Symptoms: AP, dyspnoea, acute heart failure, cardiac arrhythmia

b. ECG-changes that indicate acute ischemia

c. Development of new pathological Q-waves

d. Recent loss of myocardium or new regional dyskinesia visualized by diagnostic imaging

e. Finding of thrombus in the coronal arteries upon angiography or autopsy

STEMI is characterized by the following elevations of the ST-segment:

V2-3: ≥ 0,25 mV for men below 40 years; ≥ 0,20 mV for men above 40 years, ≥ 0,15 mV for women.

In other leads: ≥ 0,1 mV.

Newly developed LBBB should be treated as STEMI, as it indicates a new, severe coronary infarction.

Non-STEMI and UAP can have many other signs of ischemia in the ECG. In UAP these will be only transient

or related to exertion.

Treatment: For ACS, in general, time is of the essence, as the success of a possible PCI (angioplasty) treatment is highly

dependent on rapid application. Early contact to a PCI-centre is therefore essential, if STEMI is suspected, if

pain persists, if ECS reveals significant arrhythmias, or if the patient is exhibiting signs of acute heart failure

or cardiogenic shock.

As a general principle, treatment should not be delayed awaiting lab results from biomarkers, and initial

treatment should be administered based upon clinical assessment and ECG-results.

For specific treatment, please see the table on the following page.

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STEMI Non-STEMI/UAP

Acute anticoagulant

treatment

• Unfractionated heparin 7.500-

10.000 IU I.V. when transferring

to a primary PCI-centre

• If the patient is already in

anticoagulant treatment: confer

with PCI-centre, in order to

correctly reduce dose or forgo

administration.

• Fondaparinux 2,5 mg s.c. x 1 is the first

choice, low-molecular heparin is the

second choice, if eGFR > 20 ml/min.

• If eGFR ≤ 20 ml/min then use LMWH as a

half dose: inj. enoxaparin 1 mg/kg s.c. x 1

daily (max. 100 mg x 1), dalteparin 120

IU./kg x 1 s.c. (max. 10.000 IU. x 1 s.c.).

Fondaparinux is contraindicated.

• Patients who are already treated with vitamin K antagonist with INR > 2,0 or Non-Vitamin K Oral Anticoagulant should continue treatment, and not receive low molecular heparin or Fondaparinux.

Acute thrombocyte

inhibiting treatment

• Acetyl salicylic acid (ASA) 300 mg

chewed. Alternatively, ASA 150-

250 mg I.V.

• ADP-receptor blocker only

• ASA 300 mg, chewed. Alternatively, ASA

150-250 mg I.V.

• ADP-receptor blocker (ticagrelor 180 mg

or clopidogrel 600 mg).

Thrombolysis • Can be considered as an

alternative to PCI, if transport

time is significant, if patient is

unsuitable for PCI or too

unstable for transport

N/A

Pain • Nitro-glycerine sublingually 1-2 whiffs, 0,4 mg/dose, possibly followed by I.V. administration. Use with care when systolic BP is < 100 mm Hg. Nitro-glycerine is contraindicated with concurrent use of PDE-5 inhibitors (sildenafil, vardenafil within 24 hours, tadalafil within 48 hours) and when there is suspicion of right ventricle infarction.

• Morphine I.V. 2, 5-10 mg p.n., alternatively fentanyl 50-100 micrograms I.V.

• Beta-blocker orally given at low dose can be considered during continuous ischemia in Non-STEMI-patients, e.g. oral metoprolol 25 mg x 2. Contraindicated if systolic BP is < 100 mmHg, if there are signs of acute heart failure, 2nd or 3rd degree AV-block or know severe asthma. It is advised to control LVEF with echocardiography before administration.

• Contact PCI-centre acutely if pain shows to be resistant to treatment.

Hypoxemia/Dyspnoea

• Administer supplemental oxygen if saturation is < 90%. • In case of severe hypoxemia, consider intubation, and confer with an

anaesthesiologist and cardiologist

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Acute Cardiogenic Pulmonary Oedema

Definition: A condition characterized by an accumulation of fluid in the pulmonary parenchyma and alveoli, caused by

LVHF.

Pathophysiology, aetiology and pathogenesis: The condition is most often caused by a rise in pressure in the left ventricle of the heart, secondary to LVHF.

This pressure propagates to the pulmonary circulation and causes fluid to accumulate in the pulmonary

parenchyma and alveoli. It is often caused by ischemic heart disease, a direct worsening in a chronic heart

failure or a chronic or new atrial fibrillation, with diastolic dysfunction.

Patient history and symptoms: Triggers for the underlying LVEF can be infectious (especially pneumonia), shock, smoke poisoning,

arrhythmia, anaemia, endocrine disorders, anxiety and panic attacks or sodium rich diets. Patients with

acute or chronic ischemic heart disease are also at increased risk, as this can be a direct cause of heart

failure.

Most distinctive are respiratory symptoms with varying degrees of dyspnoea, sometimes accompanied by

coughing. Patients will be uneasy and frightful, as the condition is quite uncomfortable. Patients whose

heart failure stems from ACS will also often have cardiac chest pains as described in the ACS section.

Presentation upon clinical examination: The patient will appear anxious, unrestful, possibly confused, and will prefer a sitting over a lying position.

Often the patient will have tachypnoea, and may have cyanosis and lowered SAT, as well as coughing with

or without a foaming or bloody expectorate. Pulmonary auscultation will have audible coarse crepitation,

as well as expiratory wheezing. Patients will exhibit varying degrees of respiratory exhaustion.

Patients often present with jugular vein stasis as a sign of congestion. Most have a raised pulse and some a

lowered systolic BP, while some will have a compensatory high systolic BP. Severe cases will also appear

shocked with pale skin, oliguria (lowered urine production) and cold extremities.

Upon cardiac auscultation tachycardia will be audible, and any heart valve disease might be reflected in

murmurs.

Relevant acute diagnostic procedures: ECG will elucidate any possible signs of AMI or arrhythmia.

Spirometry can help rule out exacerbation of COPD, as this condition will show results more compatible

with an obstructive pulmonary disease.

Arterial blood gas analysis, including acid-base status, can help determine the level of respiratory

insufficiency.

Relevant blood tests include Hgb, thrombocytes, leukocytes, CRP, sodium, potassium, creatinine, troponins

I/T, BNP, TSH, haematological markers.

CXR can sometimes visualize alveolar oedema, pleural effusion, cardiomegaly, prominent vessels

(hypertension) as well as Kerley B lines (sign of pulmonary Oedema). CXR cannot detect early pulmonary

oedema, but can be used for differential diagnostics.

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Diagnosis: Diagnosis of pulmonary oedema is based upon patient history, clinical examination and CXR. Signs of heart

failure in these indicate that the pulmonary oedema is cardiogenic in origin.

Treatment: Central to treatment is to treat the underlying cause of the pulmonary oedema.

Pathology Treatment

• Respiratory exhaustion and unmanageable cardiac pre-load

• Elevation of the upper body to half sitting position

• SAT below 95% • Supplemental xygen therapy 5-10 L/min

• Suspected AMI with cardiac chest pain • Pharmacological treatment as described under ACS

• Overloading of the heart and congestion leading to pulmonary oedema

• Loop diuretic, e.g. furosemide I.V. 20-40 mg glyceryl nitrate 0,5 mg sublingually (only if systolic BP is above 90 mmHg)

• Respiratory exhaustion and dysfunction • CPAP or BIPAP/NIV

Honourable mentions and differential considerations:

Spontaneous pneumothorax A condition defined by spontaneous appearance of air between the parietal and visceral layer of the pleura.

It is most often seen among younger men between 20-40 years. Patients experience sudden chest pains

with dyspnoea, and the condition can be identified upon CXR.

Anaemia Anaemia is a low concentration of Hbg in the blood, despite normal hydration and volume. It is a common

comorbidity that many patients will experience. Many, otherwise healthy, patients never experience

symptoms, and those that do mainly experience fatigue. Some experience dyspnoea, though, and it can

contribute to all of the 5 five principal conditions. It is especially worth considering if the patient’s only

symptoms are fatigue and dyspnoea.

Diabetic Ketoacidosis Diabetic ketoacidosis is a condition triggered by absolute insulin deficiency and a dependence on free fatty

acids, resulting in formation of acidic ketones. This will trigger an increase in respiratory drive, producing

dyspnoea, and objectively obvious increased respiratory effort, anxiety and unrest. This can be mistaken for

several of the 5 conditions focused on above. It is therefore often worthwhile to remember checking BS.

Psychiatric disease Anxiety and panic attacks can imitate acute respiratory distress with hyperventilation and tachypnoea, as

well as unrest. They can even contribute to trigger several of the 5 conditions focused upon above, and one

might do well to keep these diagnoses in mind.

Pain Severe pain can appear reminiscent to circulatory dysfunction, as well produce an increase in respiratory

effort. With a confused, sedated or otherwise impaired patient, this can be misinterpreted as a respiratory

or cardiac problem, as the patient might appear to be dyspnoeic.

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Abbreviations, alphabetized:

ACS: Acute coronary syndrome

AMI: Acute Myocardial Infarction

AP: Angina pectoris

aPPT: Activated partial thromboplastin time

BIPAP: Bilevel positive airway pressure

BNP: Brain natriuretic peptide

BS: blood sugar

CABG: Coronary artery bypass grafting

COPD: Chronic obstructive pulmonary disease

CPAP: continuous positive airway pressure

CRP: C-reactive protein

DVT: deep vein thrombosis

FEV1: forced expiratory volume over 1 second

FVC: forced vital capacity

HDL: High-density lipoprotein

Hgb: Haemoglobin

HgbA1C: Haemoglobin A1c

I.V.: Intravenous

INR: International Normalized Ratio

IU: international units

kPa: kilopascals

LBBB: Left bundle branch block

LDL: Low-density lipoprotein

LMWH: low molecular weight heparin

LVEF: Left ventricle ejection fraction

LVHF: Left ventricular heart failure

mg: milligrams

NIV: Non-invasive ventilation

NOAC: new oral anticoagulant

Non-STEMI: Non- ST-segment elevation

myocardial infarction

NSAID: non-steroid anti-inflammatory drug

NTproBNP: N-terminal pro Brain Natriuretic

Peptide

NYHA: New York Heart Association

PaCO2: partial arterial pressure of carbon dioxide

PaO2: partial arterial pressure of oxygen

PCI: Percutaneous Coronary Intervention

PE: Pulmonary embolus

PEEP: positive end-expiratory pressure

PEF: peak flow (in expiration)

PLB: pursed lip breathing

RVHF: Right ventricle heart failure

s.c.: subcutaneously

SA: Status asthmaticus

SABA: short acting beta 2 agonist

SAMA: short acting muscarinic antagonist

SAT: peripherally measured arterial blood oxygen

sPESI: simplified pulmonary embolism severity

index

STEMI: ST-segment elevation myocardial

infarction

TSH: Thyroid-stimulating hormone

TTE: transthoracic echocardiography

UAP: Unstable Angina Pectoris

UFH: Unfractionated heparin

VTE: venous thromboembolism

EMSS2017: Dyspnoea Course Materialemss17.sats-kbh.dk/wp-content/uploads/2017/07/EMSS17-Dyspnoe… · Dyspnoea 2 emss17.sats-kbh.dk observe whether a patient can finish a sentence

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