Acute dyspnea pdf - سمنارات كروب D

Acute dyspnea

(breathlessness)

jassim adnan

• Breathlessness

dyspnoea

can be defined

as the feeling of an uncomfortable need to
breathe. It is unusual among sensations in
having no defined receptors, no localised
representation in the brain, and multiple
causes both in health (e.g. exercise) and in
diseases of the lungs, heart or muscles.

Pathophysiology

Respiratory diseases can stimulate breathing and

dyspnoea by

• stimulating intrapulmonary sensory nerves (e.g.

pneumothorax, interstitial inflammation and

pulmonary embolus),

• by increasing the mechanical load on the

respiratory muscles (e.g. airflow obstruction or

pulmonary fibrosis)

• by causing hypoxia, hypercapnia or acidosis,

• In cardiac failure, pulmonary congestion

reduces lung compliance and can also obstruct
the small airways

• Reduced cardiac output also limits oxygen

supply to the skeletal muscles during exercise,
causing early lactic acidaemia and further
stimulating breathing via the central
chemoreceptors.

presentation

History

• It is important to establish the rate of onset and

severity of the breathlessnes .Acute severe

breathlessness occur over minutes or hours

• Present of cardiovascular symptoms (chest pain,

palpitations, sweating and nausea) or respiratory

symptoms (cough, wheeze, haemoptysis, stridor).

• A previous history of repeated episodes of left

ventricular failure, asthma or exacerbations of COPD is

valuable.

• In children, the possibility of inhalation of a foreign

body or acute epiglottitis should always be considered

  The following should be assessed and documented:
•  level of consciousness
•  degree of central cyanosis
•  work of breathing (rate, depth, pattern, use of accessory muscles)
• adequacy of oxygenation (

SpO2)

•  evidence of anaphylaxis (urticaria or angioedema)
•  patency of the upper airway
•  ability to speak (in single words or sentences)
•  cardiovascular status (heart rate and rhythm, blood pressure and

degree of peripheral perfusion).

Airway obstruction, anaphylaxis and tension pneumothorax require

immediate identification and treatment.

Clinical assessment

Associated features

• pink, frothy sputum ,bi-basal crackles suggest

pulmonary edema

• Wheezes and prolonged expiration suggest

asthma and COPD

• silent resonant hemithorax suggest pneumothorax
• Severe breathlessness with normal breath sound

suggest pulmonary embolism

• Leg swelling suggest heart failure , or if

asymmetrical suggest vien thrombosis

Initial investigation

• Chest X-ray
• ECG
• Arterial blood gases
• Peak expiratory flow to assess severity

whenever possible

First three with proper history and clinical assessment

can reach the primary cause of breathlessness

mudar hazim

Acute left heart failure

• This is characterized by a reduction in left ventricular

output , increase In left ventricular diastolic pressure and
an increase in left atrial and pulmonary venous pressure.

• When the hydrostatic pressure of the pulmonary

capillaries exceeds the oncotic pressure of plasma (about
25–30 mmHg), fluid moves from the capillaries into alveoli
that lead to pulmonary edema. This stimulates respiration
through a series of autonomic reflexes, producing rapid
shallow respiration. Congestion of the bronchial mucosa
may cause wheeze (cardiac asthma).

• It is most often precipitated by

, but can be caused

, and other causes .it can occur in

previously healthy heart as well as diseased heart with

preciptiating illness

• Acute on chronic heart failure

presentation

• a

sudden onset of dyspnoea

at rest that rapidly

progresses to acute respiratory distress

• orthopnoea

and

prostration.

• Often with precipitating factors like acute MI
• The patient appears

agitated

pale

and

clammy

• Cold extremities

and

rapid pulse

, but some times

bradycardia

that may contribute in this acute episode of

• Pink frothy

blood stained sputum

• Blood pressure is

elevated

due to activation of SNS ,or

normal

low

in cardiogenic shoke

• The

JVP

is usually elevated, particularly with associated

fluid overload or right heart failure.

• A ‘

gallop

’ rhythm, with a

third heart sound

, is

heard

• A

new systolic murmur

may signify acute mitral

regurgitation or ventricular septal rupture

• Fine Basal crepitations ,

or throughout lungs if

severe case

• Expiratory wheezes

• Additional feature of chronic heart failure (in

acute on

chronic HF

)

Investigations

• Chest X-ray : increase vascularity, cardiomegaly,

thickened interlobular septa and dilated
lymphatics ( kerly B lines) , bilateral reticular
shadowing and pleural effusion

• Echocardiography to determine etiology
• ECG ,detect etiology (eg:-acute MI)
• Serum urea, creatinine and electrolytes,

haemoglobin and thyroid function determine
nature and severety of underlying disease and
complications

management

• Hospitalization

, rest

and

upright position

with continuous

heart monitoring , BP ad pulse oximetry

• IV opiate

( but give with caution )

• Oxygen high flow
• Diuretics

, (furosemide IV 50-100 mg)

• Inotropics

like dopamine or doputamine to augment

cardiac function especially in hypotensive patient

• IV nitrate infusion

or sublingual glyceryle trinitrate

• intra-aortic balloon pump

may be beneficial in patients

with acute cardiogenic pulmonary oedema and shock.

Other elements of management are summerized in

box 16.15

Pulmonary embolism

• The majority of pulmonary emboli arise from

the propagation of lower limb deep vein
thrombosis . other rare causes like septic
emboli , choriocarcinoma, fat following
fracture of long bones such as the femur, air,
and amniotic fluid, which may enter the
mother’s circulation following delivery.

presentation

investigations

• Chest X-ray
• Electrocardiogram
• Arterial blood gases

•

D-dimer test,low value

high negative predictive value

• CT pulmonary angiography is the first-line diagnostic

test

• Colour Doppler ultrasound of the leg veins in

suspected case

management

General measures

;

recuscitation
• oxygen should be given to maintain oxygen saturation

above 90%

• Intravenous fluids or plasma expander, in hypotensive

and shock patients

• Opiate to relieve pain (with caution)

Anticoagulants

(eg:-LMWH and warfarin)

Thrombolytic and surgical therapy

in case of cardiogenic

shock

Prophylaxis and long term management

saad mahmood

Acute exacerbation of asthma

• increased symptoms, deterioration in lung

function, and an increase in airway inflammation.
Exacerbations are most commonly precipitated
by viral infections but moulds ,

pollens

(particularly following thunderstorms) and

air

pollution are also implicated

• Most attacks are characterised by a gradual

deterioration over several hours to days but some
appear to occur with little or no warning: so-
called brittle asthma.

presentation

Acute severe asthma

• severe dyspnoea,
• tachypnoea (RR > 25/min),
• tachycardia (PR > 110/min),
• unable to complete a sentence in one breath
• PEF is 33%-50% of predicted (less than 200

L/min).

• PaO

(and SpO

) is usually normal

• PaCO

is low (hyperventilation)

Life threatening asthma

• The patient is unable to speak
• cyanosed, exhausted, and confused
• Bradycardia
• Silent chest and coma may follow.
• PEF is less than 33% predicted (less than 100

L/min)

• SpO

<92% (PaO

<60 mmHg).

• PaCO

: normal or raised

Management

Of acute severe and life threatening asthma

•

Oxygen

. High concentrations (humidified if possible)

maintain the oxygen saturation above 92% in adults.

• High dose nebulized bronchodilators



agonist

(salbutamol 2.5 – 5 mg) repeated within 30 minutes, +/-
nebulized ipratropium bromide

• IV hydrocortisone

200 mg or

oral prednisolone

40 -60

mg.

• Consider IV Magnesium sulphate ,

aminophylline

• Ventilatory support

(endotracheal intubation and

mechanical ventilation)

• Short course of oral corticosteroids

should be prescribed

with optimization of his medication and managing any
possible trigger factors after discharge.

Acute exacerbation of COPD

• Exacerbations are a prominent feature of the

natural history of COPD. Exacerbations are
episodes of

increasing

dyspnoea and cough and

change in

the amount

and

character

of sputum.

The frequency of exacerbations increases as the
airway obstruction increases. Exacerbations are
usually triggered by bacterial or

viral

respiratory

infections or

air pollution

. Commonly

encountered bacteria during exacerbations
include

H. influenza

Streptococcus

pneumonia

and

Moraxella catarrhalis

• The presence of

cyanosis

oedema

and

altered

level of consciousness

are indications for

hospital admission.

management

In hospital include:-
• Oxygen therapy: Controlled oxygen at 24% or 28%

should be used with the aim of maintaining a

PaO2 of

more than (60 mmHg) (or an

SaO2 of more than 90%).

• Bronchodilators: SABA (salbutamol) combined with

ipratropium bromide are nebulized with oxygen (or by
mechanical nebulizer).

• Corticosteroids: Oral prednisolone 30mg for 10 days.
• Antibiotics: are indicated in the treatment of

exacerbation in most cases. The choice usually include
penicillins or macrolides

• Consider:
• Non-invasive ventilation (NIV): if the patient failed to

respond to the above measures

• Mechanical ventilation is indicated if NIV failed, or if

the patient's consciousness is disturbed or he cannot

clear his secretions

• Additional therapies:
• Peripheral oedema may require diuretic therapy
• Respiratory stimulants like doxapram has been largely

replaced by the use of NIV, but may be useful for

selected patients with low respiratory rate

mustafa hussein

Pneumonia

• Pneumonia is as an acute respiratory illness caused by

infection of lung parenchyma associated with recently

developed radiological pulmonary shadowing that may

segmental

lobar

multilobar

. pneumonias are

usually classified as

community-

hospital-acquired

or those occurring in

immunocompromised

hosts.

‘

Lobar pneumonia

’ is a radiological and pathological

term referring to homogeneous consolidation of one or

more lung lobes, often with associated pleural

inflammation;

bronchopneumonia

refers to more

patchy alveolar consolidation associated with bronchial

and bronchiolar inflammation, often affecting both

lower lobes.

presentation

Systemic features

• , such as fever, rigors, shivering and malaise,

predominate and delirium may be present.

• Loss of appetite and headache

Pulmonary symptoms

• Cough (painful dry then with mucopurulent sputum)

,rust coloured in strep.pneumoniae

• Acute dyspnea
• Occassionally haemoptysis
• Pleuritic chest pain(may be referred to the shoulder or

anterior abdominal wall.

Atypical presentation in young and old patients

• Clinically

;

patient is

febrile ,with tachycardia ,

tachypnea with use of accessory muscles

• Cyanosis in severe cases

• Chest examination

:Dullness on percussion on

affected side or stony dull if pleural effusion present

• Auscultation : bronchial breathing , whispering

pectoriloquy ,Crackles ,vocal resonance ,friction rub

• In Elderly ,confusion
• In severely ill patient septic shock or organ failure

• Strep.pneumoniae

investigations

• Lobar pneumonia:

homogenous
consolidation of
one or more lung
lobes, often with
associated pleural
effusion

• Bronchopneumonia:

patchy alveolar

consolidation

associated with

bronchial

inflammation, often

affecting lower

lobes.

management

• Oxygen therapy ; high flow , maintain PaO2

around 60 mmHg (or SpO2 at 92%)

• Mechanical ventilation if remain hypoxic despite

oxygen therapy

• Fluid balance ; oral fluid ,or IV fluid in case of

vomiting or severely ill patient, vasopressors if
septic shock

• Antibiotic therapy ;
Inpatients:
• A respiratory quinolone (oral or IV) (OR)
• A β-lactam (co-amoxiclav 1-2 gm three time daily

IV or cefotaxime 1-2gm IV three time daily or

ceftriaxone 1-2 gm IV daily) PLUS, a macrolide

(oral or IV)

(If

Staphylococcus aureus

is suspected, add

vancomycin or linezolid).

• Pleuritic pain is treated with paracetamol or

NSAID.

• Physiotherapy to assisst expectoration.

russel mikdad

Pneumothorax

• Pneumothorax is the presence of air in the

pleural space, which can either occur
spontaneously, or result from iatrogenic injury
or trauma to the lung or chest wall

classification

Types of spontaneous pneumothorax

presentation

• sudden-onset unilateral pleuritic chest pain or

breathlessness.

• In patient with unlderlying lung disease

breathlessness are severe

• Small pneumotharax : normal physical findings
• Larger one (> 15% of the hemithorax) decreased

or absent breath sounds

• The combination of absent breath sounds and a

resonant percussion note is diagnostic of
pneumothorax.

• in

tension pneumothorax

there is rapidly

progressive breathlessness associated with a
marked tachycardia, hypotension, cyanosis
and tracheal displacement away from the side
of the silent hemithorax.