Download ACUTE DYSPNOEA - The Medical Post

ALOK SINHA
Department of Medicine
Manipal College of Medical Sciences
Pokhara, Nepal
30.7.09 (9.00 pm)
Same patient next day morning
CAUSES
COPD-acute exacerbations
 Pulmonary oedema
 Pneumo-thorax
 Br. asthma
 Pneumonia
 Pulmonary Embolism
 Anaphylactic reaction
 Acute Laryngeal Obstruction
a. oedema
b. Foreign body
 Anxiety Neurosis

Difference between
cardiac asthma
and
COPD
History

Hypertension or valvular  S/O of COPD or asthma
heart diseases
Clinical examination
High B.P.
 Pulsus alternans
 C/F of LVH
 Predominant basal
crepts

Pulsus paradoxus
 C/F of emphysema
 Predominant expiratory
rhonchi (wheeze)

Pulmonary oedema
.
Cardiogenic -LV failure due to
 Myocardial infarction, ventricular septal rupture
following infarction
 Valvular: acute aortic regurgitation, acute mitral
regurgitation, severe aortic stenosis
 Severe hypertension
 Acute arrhythmia
 Acute myocarditis
 Acute volume overload
 Cardiomyopathy

Why the patient with pulmonary oedema
is breathless ?
Non Cardiogenic
.
Increased pulmonary capillary
permeability
Acute respiratory distress syndrome
(ARDS) -PAWP < 18 mm
International criteria
1. Acute onset of symptoms
2. The ratio of the arterial partial
pressure of oxygen (PaO2) to the
fraction of inspired oxygen (FIO2)
of 200 mm Hg or less
For Example normal PaO2 = 100, FiO2 = 20% or 1/5 so the
above ratio = 100/1/5 = 500 mm Hg
3.Bilateral infiltrates on CXRs
4.Pulmonary arterial wedge pressure
of 18 mm Hg or less or no clinical
signs of left atrial hypertension
causes of mediator release leading to
ARDS

Sepsis/pneumonia
• secondary risk factors

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alcoholism
cigarette smoking
Gastric aspiration
lung trauma due to smoke inhalation
fat emboli
direct effects of large amounts of necrotic
tissue
Less common causes

Post-bone marrow transplant

Drug overdose -
tricyclic antidepressants, opiates,
cocaine, aspirin

Near drowning

Following upper airway obstruction;
mechanism unclear

Acute form of Interstitial Pneumonia. Also
known as acute Hamman-Rich syndrome
Indirect (non-pulmonary) injury

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Shock
Septicaemia
Amniotic or fat embolism
Acute pancreatitis
Massive haemorrhage
Multiple transfusions
DIC
Massive burns
Major trauma
Head injury
• Raised ICP
• Intracranial bleed


Cardio-pulmonary bypass
Acute liver failure
.
airway obstruction
laryngeal obstruction
tumor
 infections
 oedema
 foreign body

What is the most charecteristic feature of laryngeal obstruction
?
.
Coronary artery disease
-May present without chest pain
“anginal equivalent”
Pulmonary embolism
Venous stasis -immobility
endothelial damage

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recent trauma
surgery
burns
indwelling catheters
IV drug use.
hypercoagulability
malignancy
obesity
pregnancy
HRT/OCP
BTS pre-test clinical probability scoring

Patient has clinical features compatible
with PE:
• raised respiratory rate
• ± haemoptysis
• ± pleuritic chest pain.

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Plus 2 other factors:
• 1. Absence of another reasonable clinical explanation
• 2. Presence of a major risk factor
A. plus 1 and 2: HIGH pre-test clinical probability
A. plus 1 or 2: INTERMEDIATE pre-test clinical
probability
A. alone: LOW pre-test clinical probability
Severity of Br. Asthma
Symptoms noct. Sympt
• Stage 4
Continuous
Frequent
Severe
• Stage 3
Daily
Moderate
• Stage 2
Mild
>1 /week
but <1time/day
>1 time /week
>2 times
a month
• Stage 1 <1 time /week <2 times
Intermittent
a month
FEV1/PEFR
<60% predicted
variability >30%
60-80% predicted
variability >30%
>80% predicted
variability 20-30%
>80% predicted

severe Asthma

Life-threatening asthma

Near-fatal asthma
severe Asthma

PEF 30- 50% best or predicted

Respiratory rate >25/min

Tachycardia: heart rate >100/min

Inability to complete sentences in
one breath
Life-threatening asthma


Severe airways obstruction
•PEF <33% best or predicted
•Soft breath sounds or silent chest
•Feeble respiratory effort
Increased work of breathing &
haemodynamic stress
•Exhaustion
•Hypotension (systolic BP
<100mmHg)


Ventilation-perfusion
mismatch
•Cyanosis
•Hypoxia (SpO2 <92% and/or
PaO2 50mm irrespective of
inspired O2 concentration)
Ventilatory failure
•Rising PaCO2
•Confusion or coma
Near-fatal asthma


Raised PaCO2
immediate requirement for
ventilation with raised inflation
pressures
Management
Oxygen



Oxygen is the primary therapeutic
modality
-corrects V/Q mismatch.
-provided via nasal cannula or face
masks
In significant hypoxemia
nonrebreathing masks may be used to
deliver as much as 98% oxygen
Goal of supplemental oxygen therapy
is an oxygen saturation above 92%
Non rebreathing mask
Inhaled beta-agonists
Salbutamol
Albuterol & Levalbuterol
Terbutaline
•
•
•
•
mainstays of acute therapy in asthma.
They act via stimulation of cyclic (AMP)–
mediated bronchodilation.
stimulation of receptors relaxes airway
smooth
muscles
increases mucociliary clearance &
decreases mucous production.
Anticholinergics



act via inhibition of cyclic guanosine
monophosphate (GMP)–mediated
bronchoconstriction.
-decrease mucus production
-improve mucociliary clearance
Ipratropium bromide -agent of
choice.
In severe airflow obstruction
- combination of ipratropium and
salbutamol/albuterol provide better
broncho dilatation than used alone.
Corticosteroids
Hydrocortisone
 Methylprednisolone
decrease airway inflammation and
swelling.
potentiate the effects of beta-agonist
agents improve capillary leak.
 administered intravenously or orally.
-Used mostly I.V.during status
asthmaticus

Further therapy
Magnesium sulphate


Magnesium can relax smooth muscle and
hence cause bronchodilation by
competing with calcium at calciummediated smooth muscle binding sites.
The published doses used range from 2575 mg/kg infused over 20 minutes, with
a maximum of 2-2.5 g/dose.
Intravenous beta-agonists
patients with refractory status
asthmaticus may respond to intravenous
administration of beta-agonists.
.

• Intravenous terbutaline albuterol or
salbutamol. i.v. terbutaline 0.4 - 10
mcg/kg/min
• dose administered should be titrated to effect
and adverse cardiac effects (tachycardia,
arrhythmias, hypokalemia)

monitoring of cardiac enzyme levels in
patients receiving prolonged intravenous
beta-agonists
Ketamine
Ketamine is a short-acting
pentachlorophenol (PCP) derivative
bronchodilatory effects
increases endogenous catecholamine
levels
Acts as a sedative to reduce anxiety and
agitation that can exacerbate tachypnea
and work of breathing
useful in small children with status
asthmaticus
.
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Methylxanthines
.
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role of methylxanthines -Theophylline or
Aminophylline(theophylline &
ethylenediamine in 2:1 ratio) is now
debated.
have many undesirable adverse effects,
such as nausea and vomiting.
studies have failed to show additional
benefit when methylxanthines are
administered to patients who are already
receiving frequent beta-agonists and
steroids
• recent studies have examined methylxanthines
theophylline and aminophylline and
demonstrated improvement in the clinical
asthma scores when compared with placebo
control. The theophylline effects are
• bronchodilatation,
• increased diaphragmatic function
• central stimulation of breathing
Continuous positive airway pressure (CPAP)
Indications for intubation and
mechanical ventilation
.



Apnea or respiratory arrest
Diminishing level of consciousness
Impending respiratory failure marked by
 significantly rising PCO2 with fatigue
 decreased air movement
 altered level of consciousness

Significant hypoxemia that is poorly
responsive or unresponsive to
supplemental oxygen therapy alone
Considerations in mechanical
ventilation
• Positive pressure ventilation in asthma
Complicated by severe airway obstruction &
air trapping resulting in hyperinflated lungs
resisting further inflation & places patient
at high risk of barotrauma
• mechanical ventilation should be
undertaken only in the face of continued
deterioration despite maximal broncho
dilatory therapy
• prolongation of the time needed for lung
units to fill and empty.
• Slow ventilator rates are usually needed
• principle of mechanical ventilation of
status asthmaticus is controlled
hypoventilation, tolerating higher levels
of PCO2 in order to minimize tidal
volume and peak inspiratory pressures
.
• Permissive hypercapnia can be
tolerated as long as the patient remains
adequately oxygenated
Tension pneumothorax
Emergent needle decompression


Administer 100% oxygen, and ventilate if
necessary
Locate anatomic landmarks and quickly prepare
the area to be punctured with an iodine-based
solution (eg, Betadine)

Insert a large-bore (ie, 14-gauge or 16gauge) needle with a catheter into the
second intercostal space, just superior
to the third rib at the midclavicular line,
1-2 cm from the sternal edge (to avoid
injury to the internal thoracic artery)

Use a 3-6 cm long needle, and hold it
perpendicular to the chest wall when
inserting

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Once the needle is in the pleural space,
listen for the hissing sound of air escaping
and remove the needle while leaving the
catheter in place
Secure the catheter in place, and install a
flutter valve
Prepare the patient for tube thoracostomy.
Tube thoracostomy
• Tube thoracostomy is the definitive
treatment fortension pneumothorax
• needle decompression followed up
immediate with tube thoracostomy
• hemothorax along with tension
pneumothorax is common
• Monitor the patient continuously for
arterial oxygen saturation
Comparison
COPD
Vs
Br. Asthma

airflow obstruction due Chronic obstruction of
to inflammation &
lung airflow which is
increased airway
permanent &
hyper-responsive ness
progressive over time
& bronchospasm which
is
variable over short
periods of time
 reversible with
treatment
cause
Mostly by allergens in
 Due to the chemical
atopic persons
irritation of the airways
caused by smoke(ing)


Age group

Mostly affects the young
people
 Disease of middle aged &
elderly

Pathogenesis
Airway obstruction due to  Due to
• Smooth muscle spasm
• oedema
• Loss of elastic recoil
• Remodeling of the air way
Clinical features

Chest normal in
between the attacks

Features of air way
obstruction always
seen
Complications


Emphysematous
changes do not occur
Does not progress to
cor pulmonale or type
II respiratory failure


Seen after some
years
Many cases develop
these complication
Pulmonary Function Test
Obstructive picture +
1. FEV1 ≥ 15% (and 200 ml)
increase following
administration of a
bronchodilator/trial of
corticosteroids
2. > 20% diurnal variation on ≥
3 days in a week for 2 weeks
on PEF diary
3. FEV1 ≥ 15% decrease after 6
mins of exercise
Obstructive pattern +
1.
Minimal bronchodilator
reversibility (<15%, usually
<10%)
2.
< 20% diurnal variation on ≥
3 days in a week for 2 weeks
on PEF diary
No change in FEV1: FVC with
exercise (absence of exercise
induced bronchospasm)
3.
X ray chest

Normal in between attacks.
Hyper inflated lungs at the
time of acute attack

Shows
•
•
Emphysematous changes
with bullae
Features of pulmonary
hypertension
Hoover's sign



refers to the inspiratory retraction of the
lower intercostal spaces
results from alteration in dynamics of
diaphragmatic contraction due to
hyperinflation resulting in traction on the
rib margins by the flattened diaphragm
Seen in up to 70% of patients with
severe obstruction can be an excellent
marker for severe airway obstruction