Shortness of breath

Approach to Shortness of Breath….
at Emergency Department
Presented by
Dr.Ahmed Shahed
Holy Family Red Crescent Medical College Hospital
RMO, Medicine Department
(Green Unit)

67-year-old man.
Smoke two packs of
cigarettes a day.
Stopped smoking six
years ago.
Retired coffee
salesman.
Married. No pets.
Drinks little alcohol. No other illnesses.

Shortness of
breath due to
effort.
Trouble breathing
while sitting still.
Productive cough with
green sputum.
Looks pale, feels as his
temperature is raised.
No shivers, sore
throat, vomiting,
diarrhea, and not sick.

Thin with
broad chest
Moderate SOB
Trachea is
positioned in
the midline
Thorax moves
up & down
symmetrically
Breathing rate
is 32 per min
Reduced
breath sound
across lung
Wheezing on
expiration

Extended
expiration
BP 132/78
mmHg
Heart rate 94
per min
Arterial oxygen
saturation 91%
Decreased FVC
& FEV1
Increase TLC,
FRC & RV

Cardiac Pulmonary
Mixed
cardiac or
pulmonary
non-cardiac
non-
pulmonary

COPD Asthma
Restrictive
Lung
Disorders
Hereditary
Lung
Disorders
Pneumonia
Pneumo-
thorax

Congestive
Heart Failure
(CHF)
Coronary Artery
Disease (CAD)
Recent or past
history of
Myocardial
Infarction (MI)
Cardiomyopathy
Valvular
dysfunction
Left
ventricular
hypertrophy
Pericarditis Arrhythmias

COPD with
pulmonary
HTN and/or
cor pulmonale
Deconditioning
Chronic
pulmonary
emboli
Pleural
effusion

Metabolic
conditions
(e.g. acidosis)
Pain Trauma
Neuromuscular
disorders
Functional
(anxiety, panic,
hyperventilation)
Chemical
exposure

Asthma COPD Pneumonia
Congstive heart
failure
Anxiety, panic,
hyperventilation

© Global Initiative for Asthma
Features that (when present) favor
asthma or COPD
GINA 2014, Box 5-2B (3/3)
Feature Favors asthma Favors COPD
Age of onset qBefore age 20 years qAfter age 40 years
Lung function qRecord of variable airflow limitation
(spirometry, peak flow)
qNormal between symptoms
qRecord of persistent airflow limitation
(post-BD FEV1/FVC <0.7)
qAbnormal between symptoms
Past history or
family history
qPrevious doctor diagnosis of asthma
qFamily history of asthma, and other allergic
conditions (allergic rhinitis or eczema)
qPrevious doctor diagnosis of COPD,
chronic bronchitis or emphysema
qHeavy exposure to a risk factor: tobacco
smoke, biomass fuels
Chest X-ray qNormal qSevere hyperinflation
Time course qNo worseningof symptoms over time.
Symptoms vary seasonally, or from year to
year
qMay improve spontaneously, or respond
immediately to BD or to ICS over weeks
qSymptomsslowly worsening over time
(progressive course over years)
qRapid-acting bronchodilator treatment
provides only limited relief
Pattern of
respiratory
symptoms
qSymptoms vary overminutes, hours or days
qWorse during night or early morning
qTriggered by exercise, emotions including
laughter, dust, or exposure to allergens
qSymptoms persist despite treatment
qGood and bad days, but always daily
symptoms and exertional dyspnea
qChronic cough and sputum preceded
onset of dyspnea, unrelated to triggers

Step 3 - Spirometry
Spirometric variable Asthma COPD ACOS
Normal FEV1/FVC
pre- or post-BD
Compatible with asthma Not compatible with
diagnosis (GOLD)
Not compatible unless
other evidence of chronic
airflow limitation
FEV1 =80% predicted Compatible with asthma
(good control, or interval
between symptoms)
Compatible with GOLD
category A or B if post-
BD FEV1/FVC <0.7
Compatible with mild
ACOS
Post-BD increase in
FEV1 >12% and 400mL
from baseline
High probability of
asthma
Unusual in COPD.
Consider ACOS
Compatible with
diagnosis of ACOS
Post-BD FEV1/FVC <0.7 Indicatesairflow
limitation; may improve
Required for diagnosis
by GOLDcriteria
Usual in ACOS
Post-BD increase in
FEV1 >12% and 200mL
from baseline (reversible
airflow limitation)
Usual at some time in
courseof asthma; not
always present
Common in COPD and
more likely when FEV1 is
low, but consider ACOS
Common in ACOS, and
more likely when FEV1 is
low
FEV1 <80% predicted Compatible with asthma.
A risk factor for
exacerbations
Indicates severity of
airflow limitation and risk
of exacerbations and
mortality
Indicates severity of
airflow limitation and risk
of exacerbations and
mortality
GINA 2014, Box 5-3

Initial assessment –the role of
symptoms, signs and measurements
Clinical features Clinical features can identify some patients with severe asthma,
e.g. severe breathlessness, tachypnea, tachycardia, silent chest,
cyanosis, accessory muscle use, altered consciousness or collapse.
None of these singly or together is specific. Their absence does not
exclude a severe attack.

PEF or FEV1 Measurements of airway calibre improve recognition of severity and
guide hospital or at home management decisions. PEF is more
convenient and cheaper than FEV1. PEF as % previous best value or
% predicted most useful

Pulse Oximetry Necessary to determine adequacy of oxygen therapy and need
for arterial blood gas measurement. Aim of oxygen therapy is to
maintain SpO2 92%

Pulse oximetry Necessary to determine adequacy of oxygen therapy and need for
arterial blood gas measurement. Aim of oxygen therapy is to
maintain SpO2 92%
Blood gases (ABG) Necessary for patients with SpO2<92% or other features of life
threatening asthma

Chest X-ray Not routinely recommended in patients in the absence of:
•suspected pneumomediastinum or pneumothorax
•suspected consolidation
•life threatening asthma
•failure to respond to treatment satisfactorily
•requirement for ventilation
Systolic paradox Abandoned as an indicator of the severity of an attack
Near fatal asthma Raised PaCO2and/or requiring mechanical ventilation with raised
inflation pressures

Life threatening asthma Any one of the following in a patient with severe asthma:
•PEF <33% best orpredicted
•SpO2<92%
•PaO2<8 kPa
•normal PaCO2(4.6-6.0 kPa)
•silent chest •cyanosis •feeble respiratory effort
•bradycardia •dysrhythmia •hypotension
•exhaustion •confusion •coma

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
Moderate asthma exacerbation
•Increasing symptoms
•PEF >50-75% best or predicted
•No features of acute severe asthma
Brittle asthma
•Type 1: wide PEF variability (>40% diurnal variation for >50% ofthe time over a period >150
days) despite intense therapy
•Type 2:sudden severe attacks on a background of apparentlywell-controlled asthma

Patients at risk of developingnear fatal
or fatal asthma
Asthma and Adverse behavioural orpsychosocial features
recognised by one or more of:
•previous near fatal asthma
(previous ventilation or respiratory
acidosis)
•previous asthma admission
•requiring 3 classes of asthma
medication
•heavy use of ß2agonist
•repeated attendances at A&E for
asthma care
•brittle asthma
recognised by one or more of:
•non-compliance with treatment or monitoring
•failure to attend appointments
•self-discharge from hospital
•psychosis, depression,other psychiatric illness or
deliberate self-harm
•current or recent major tranquilliser use
•denial
•alcohol or drug abuse
•obesity
•learning difficulties
•employment problems
•income problems
•social isolation
•childhood abuse
•severe domestic,marital or legal stress

Measure Peak Expiratory Flow and Oxygen Saturation
Moderate Acute Severe Life Threatening
Scottish Intercollegiate Guidelines Network
British Guideline on the Management of Asthma
Salbutamol- 4 puffs
then 2/ 2min up to
10 via spacer
Salbutamol 5mg via
nebulizer
Contact ICU if life-
threatening features
present
Time: 0-5 minutes

In-text: (Scottish Intercollegiate Guidelines Network, 2014)
Clinically
Stable,
PEF>75%
Clinically
stable,
PEF,75%
No life-
threatening
features,
PEF 50-75%
Life-
threatening
features or
PEF< 50%
O2 to maintain
SPO2 94-98%
Salbutamol 5mg
+ ipratropium
0.5mg via
nebulizer
Prednisolone 40-
50 mg orally or
100 mg IV
hydrocortisone
Measure Arterial
Blood Gasses
Repeat Salbutamol
5mg nebulizer.
Prednisolone 10-
50mg orally.
Possible
discharge
Time 15-20 mins

Patient
recovering
PEF > 75%
No signs of
severe
asthma
PEF 50-75%
Signs of
severe
asthma
PEF <50%
Salbutamol 5 mg
+ ipratropium 0.5 mg
via nebuliser
After 15 minutes
ƒconsider continuous
salbutamol
nebuliser 5-10 mg/hr
ƒConsider IV
magnesium sulphate
1.2-2 g over 20
minutes
ƒCorrect
fluid/electrolytes,
especially K+
disturbances
ƒChest X-ray
ƒRepeat ABG
Observe and Monitor:
-SpO2
-Heart Rate
-Resp Rate
Potential Discharge
Time 60 mins

Bibliography: Scottish Intercollegiate Guidelines Network, (2014). British Guideline on the Management of Asthma. London: British Thoracic
Patient stable
PEF > 50%
Signs of severe
asthma or PEF
<50%
Admit
Patient
accompanied by
nurse or doctor at
all times
Potential
discharge
Time 120 mins

Definition of COPD
• Airflow obstruction is defined as reduced FEV1/FVC ratio (< 0.7)
• It is no longer necessary to have an FEV1 < 80% predicted for definition of
airflow obstruction
• If FEV1 is ≥ 80% predicted, a diagnosis of COPD should only be made in the
presence of respiratory symptoms, for example breathlessness or cough
• COPD produces symptoms, disability and impaired quality of life which may
respond to pharmacological and other therapies that have limited or no
impact on the airflow obstruction.
FEV1 = forced expiratory volume in 1 second
FVC = forced vital capacity

Global Strategy for Diagnosis, Management and Prevention of COPD
Risk Factors for COPD
Genes
Infections
Socio-economic
status
Aging Populations
© 2015 Global Initiative for Chronic Obstructive Lung Disease

Diagnose COPD: Spirometry
– Perform spirometry if COPD seems likely [2004]
– The presence of airflow obstruction should be confirmed by performing
post-bronchodilator spirometry [new 2010]
– Consider alternative diagnoses or investigations in:
• - older people without typical symptoms of COPD
where the FEV1/FVC ratio is < 0.7
• - younger people with symptoms of COPD where the
FEV1/FVC ratio is ≥ 0.7 [new 2010]
– All health professionals involved in the care of people with COPD should
have access to spirometry and be competent in the interpretation of the
results [2004]

Differentiating COPD from
asthma: 2
• If diagnostic uncertainty remains, the following findings should be used
to help identify asthma:
• - FEV1 and FEV1/FVC ratio return to normal with drug therapy
• - a very large (>400ml) FEV1 response to bronchodilators or to
30mg prednisolone daily for 2 weeks
• - serial peak flow measuremenst showing significant (20% or
greater) diurnal or day-to-day variability
• - remaining diagnostic uncertainty may be resolved by referral
for more detailed investigations
• [2004]

Diagnose COPD: assessment of
severity
• Assess severity of airflow obstruction using reduction in FEV1
NICE clinical
guideline 12
(2004)
ATS/ERS 2004 GOLD 2008 NICE clinical
guideline 101
(2010)
Post-
bronchodilator
FEV1/FVC
FEV1 %
predicted
Post-
bronchodilator
Post-
bronchodilator
Post-
bronchodilator
< 0.7 80% Mild Stage 1 (mild) Stage 1 (mild)*
< 0.7 50–79% Mild Moderate Stage 2 (moderate) Stage 2 (moderate)
< 0.7 30–49% Moderate Severe Stage 3 (severe) Stage 3 (severe)
< 0.7 < 30% Severe Very severe Stage 4 (very
severe)**
Stage 4 (very
severe)**
* Symptoms should be present to diagnose COPD in people with mild airflow obstruction
** Or FEV1 < 50% with respiratory failure
[new 2010]

Oxygen: titrate to improve the patient’s hypoxemia with a target saturation of 88-92%.
Bronchodilators: Short-acting inhaled beta2-agonists with or without short-acting
anticholinergics are preferred.
Systemic Corticosteroids: Shorten recovery time, improve lung function (FEV1) and arterial
hypoxemia (PaO2), and reduce the risk of early relapse, treatment failure, and length of
hospital stay. A dose of 40 mg prednisone per day for 5 days is recommended. Nebulized
magnesium as an adjuvent to salbutamol treatment in the setting of acute exacerbations of
COPD has no effect on FEV1.
Manage Exacerbations: Treatment Options

• FEV1/FVC < 0.70
• FEV1 ≥ 80% predicted
• FEV1/FVC < 0.70
• ≤ FEV1 50-80% predicted
• FEV1/FVC < 0.70
• ≤ FEV1 30- 50% predicted
• FEV1/FVC < 0.70
• FEV1 < 30% predicted or
FEV1 < 50% predicted plus
chronic respiratory failure
Add regular treatment with long-acting bronchodilators; Begin Pulmonary Rehabilitation
Add inhaled glucocorticosteroids if repeated acute
exacerbations
Add LTOT for chronic
hypoxemia.
Consider surgical options
III: SevereI: Mild
II: Moderate
IV: Very Severe
Active reduction of risk factor(s); smoking cessation, flu vaccination
Add short-acting bronchodilator (as needed)

• Pneumonia is an inflammation of the lung
parenchyma (i.e. alveoli rather than the
bronchi) of infective origin.
Pneumonia 46

Classified based on two types
1. Type 1
• Lobar pneumonia
• Bronchopneumonia
2. Type 2
• Community- acquired pneumonia (CAP)
• Hospital-acquired pneumonia (HAP)
Pneumonia 47

Pneumonia 48
Lobarpneumonia
Consolidation
confined to
one or more
lobes (or
segments of
lobes) of
lungs.

Pneumonia 49
Bronchopneumonia
•Patchy
consolidation
usually in the
bases of both
lungs.

• Adequacy of respiratory function
• Humidified oxygen for hypoxemia
• Bronchodilators (albuterol)
• Chest physiotherapy with postural drainage
• Adequate hydration if necessary
• Expectorants such as guaifenesin
• Chest pain- analgesics
Pneumonia 50

ACCF/AHA Stages of HF NYHA Functional Classification
A At high risk for HF but without structural
heart disease or symptoms of HF.
None
B Structural heart disease but without signs
or symptoms of HF.
I No limitation of physical activity.
Ordinary physical activity does not cause
symptoms of HF.
C Structural heart disease with prior or
current symptoms of HF.
I No limitation of physical activity.
Ordinary physical activity does not cause
symptoms of HF.
II Slight limitation of physical activity.
Comfortable at rest, but ordinary physical
activity results in symptoms of HF.
III Marked limitation of physical activity.
Comfortable at rest, but less than ordinary
activity causes symptoms of HF.
IV Unable to carry on any physical activity
without symptoms of HF, or symptoms of
HF at rest.
D Refractory HF requiring specialized
interventions.

Classifications of AHFS after AMI utilized in CCU and
ICCU
• Stage I—No clinical signs of HF.
• Stage II—Heart failure. Rales,S3 gallop and pulmonary
venous hypertension.
• Stage III—Severe HF. Frank pulmonary oedema with rales
throughout the lung fields
• Stage IV—Cardiogenic shock.Hypotension (SBP <90
mmHg), peripheral vasoconstriction (oliguria, cyanosis
diaphoresis) .

• Diagnosis of AHF is based on the symptoms and clinical
findings,
• Supported by appropriate investigations such as ECG, chest X-
ray, biomarkers, and Doppler echocardiography

• CXR- Cardiomegaly,Kerley’s A, B lines, pulmonary
congestion-bat wings haziness, Cephalization of veins,
pleural effusions

• Biomarker of HF NP-useful in
diagnosis,assessing severity
predicting short & long-term CVS
mortality
• No HF- BNP <100pg/dl , PRO-
BNP < 300pg/dl
• HF- BNP >500pg/dl , PRO-BNP
>1000pg/dl
• 80% Sensitivity for heart failure
• CBC, SE, KFT, LFT, RBS, lipid
profile, thyroid function test, CKMB,
cardiac TnI/TnT,
• MRI-Gold standard for assesing
cardiac mass or volume
• Nuclear Studies-Exercise or
pharmacologic stress nuclear
SPECT imaging with thallium
201 or Tc 99 may detect ischemia
or previous MI and also assess LV
function.
• Pulmonary artery catheter may be
necessary in selected patients to
obtain a more accurate and
comprehensive hemodynamic
profile during hospitalization

• ECG- LA enlargement ,arrhythmias , LVH, previous MI
• Echocardiography-assesment of systolic / diastolic
function, EF calculation ,any valvular abnormality
,abnormal wall motion

Management in the emergency dept.
• Diagnosis and treatment are usually carried out in parallel,
• Close monitoring of the patient’s vital functions is essential during the initial
evaluation and treatment

Pharmacological therapy in acute
management
• Oxygen should be given to all hypoxaemic pts
maintain SpO2 95–98%
• Patent airway should be ensured and FiO2 can be
increased
• In non-hypoxaemic patients it causes vasoconstriction
and a reduction in cardiac output.

Diuretics use
• Indicated in symptoms secondary to fluid retention.
• Most patients with dyspnoea in AHF caused by pulmonary
oedema
• Rapid symptomatic relief by immediate venodilator action and
subsequent removal of fluid.
• Start with individualized dose depending on clinical condition

Diuretic dosing and administration

Opiates(Morphine)
• Indicated in early stage of severe AHF associated
with restlessness and dyspnoea.
• Morphine induces venodilatation and mild arterial
dilatation, and reduces heart rate
• Morphine sulfate  2-5 mg iv over 2-3 mins and can
be repeated every 10 to 25 mins until effect is seen
• Opiates induce nausea and depress respiratory drive
potentially increasing the need for invasive
ventilation

Vasodilators
• First line therapy in AHF with an adequate BP and signs of
congestion with low diuresis
• Nitrates causes venous and arterial balanced
vasodilation,reduce LV pre-load and after-load, without
impairing tissue perfusion.
• Sodium nitroprusside used in severe HF with predominantly
increased after-load (hypertensive HF or MR)
• Nesiritide-Recombinant human BNP with venous, arterial, and
coronary vasodilatory properties reduce preload and after-load,
increase CO without direct inotropic effects.
• Calcium antagonists-Not recommended in treatment of AHF

Indications and dosing of vasodilators in AHF

Inotropes
• Reserved for pts with severely reduced cardiac output
compromised vital organ perfusion
• Inotropes cause sinus tachycardia and may induce myocardial
ischaemia and arrhythmias.
• There is long-standing concern that they may increase
mortality
• Levosimendan, milrinone can counteract the effect of a beta-
blocker

Vasopressors
• In cardiogenic shock.
• When the combination of inotropic agent and fluid challenge
fails to restore adequate arterial pressure and organ perfusion.
• Peripheral arterial vasoconstrictor action raise blood pressure
and redistribute cardiac output from the extremities to the vital
organs.
• It may increase the after-load of a failing heart and further
decrease end-organ blood flow

Drugs used to treat AHF that
are positive inotropes or vasopressors or both

Other pharmacological therapy
• Cardiac glycosides – used in AF induced heart failure with
insufficient ventricular rate-control by b-blockers.
• IV Beta Blocker should not be started during the initial phase
of AHFS as acutely decrease cardiac contractility.
• However, a short-acting IV agent(esmolol) may be considered
when AHF is ppt. by AF or flutter with a rapid ventricular
response
• Anticoagulation-in ACS with or without HF, in AF and to
prevent thrombo-embolism.

Non-pharmacological therapy
• Restrict Na intake 2g/day and fluid intake 1.5–2.0 l/day
• Non-invasive ventilation- CPAP/NIPPV used when increased
FiO2 fail to improve tissue oxygenation.
• Endotracheal intubation and invasive ventilation- Reverse
AHF-induced respiratory muscle fatigue, acute respiratory
failure not responding to vasodilators/oxygen
therapy/CPAP/NIPPV.
• Mechanical circulatory support- IABP,VAD
• Venovenous isolated ultrafiltration reserved for diuretics
resistant/unresponsive cases

Carpopedal spasm occurs when acute hypocarbia causes reduced
ionized calcium and phosphate levels, resulting in involuntary
contraction of the feet or (more commonly) the hands .

• Upon a first attack of acute HVS, the diagnosis
depends on recognizing the typical constellation of
signs and symptoms and ruling out the serious
conditions that can cause the presenting symptoms.
• Acute coronary syndrome (ACS) and pulmonary
embolism (PE) are the 2 most common serious
entities that may present similarly to HVS.
• Clinical assessment is sufficient to rule these out.
• A standard workup for atypical chest pain, including
pulse oximetry, chest radiography, and ECG, may still
be warranted depending on the clinical picture.

• Patients with a history of HVS who have undergone an
appropriate workup at some earlier time may not need
any further laboratory evaluation in the setting of a
recurrence. Recognition of the typical constellation of
dyspnea, agitation, dizziness, atypical chest pain,
tachypnea and hyperpnea, paresthesias, and carpopedal
spasm in a young, otherwise healthy patient with an
adequate prior evaluation is sufficient to make the
diagnosis.
• A low pulse oximetry reading in a patient who is
hyperventilating should never be attributed to HVS. The
patient should always be evaluated for other causes of
hyperventilation.

• ABG is indicated if any doubt exists as to
the patient’s underlying respiratory status;
it may be helpful when HVS-induced
acidosis is suspected, or when shunting or
impaired pulmonary gas exchange is
considered.

• ABG sampling confirms a compensated
respiratory alkalosis in a majority of cases.
The pH is typically near normal, with a low
PaCO2 and a low bicarbonate level.
• ABG sampling is also useful in ruling out
toxicity from carbon monoxide poisoning,
which may present similarly to HVS.
• Toxicology screening is indicated.
• If acute PE is being considered, ELISA D-
dimer assay may be helpful.

• Imaging studies are not indicated when
the diagnosis of HVS is clear.
• Because PE can present with findings
identical to those of HVS, a first-ever
episode of acute HVS may warrant V/Q
scanning or CT pulmonary angiography to
rule out perfusion defects.
• Chest radiography is indicated for patients
who are at high risk for cardiac or
pulmonary pathology.

Breathing Techniques
• Rebreathing into a paper bag is no longer a recommended
technique, because significant hypoxia and death have been
reported
• . Moreover, carbon dioxide itself may be a chemical trigger for
anxiety in these patients.
• Simple reassurance and an explanation of how hyperventilation
produces the patient’s symptoms are usually sufficient to
terminate the episode.
• Provoking the symptoms by having the patient voluntarily
hyperventilate for 3-4 minutes often convinces the patient of the
diagnosis.

Breathing Techniques
• Most patients with HVS tend to breathe with the upper
thorax and have hyper-inflated lungs throughout the
respiratory cycle. Because residual lung volume is high,
they are unable to achieve full tidal volume and
experience dyspnea.
• Physically compressing the upper thorax and having
patients exhale maximally decreases hyperinflation of
the lungs.
• Instructing patients to breathe abdominally, using the
diaphragm more than the chest wall, often leads to
improvement in subjective dyspnea and eventually
corrects many of the associated symptoms.

What is “calm breathing”?
• Calm breathing (sometimes called “diaphragmatic
breathing”) is a technique that helps you slow down your
breathing when feeling stressed or anxious.
• Newborn babies naturally breathe this way, and singers,
wind instrument players, and yoga practitioners use this
type of breathing.
• Diaphragmatic breathing slows the respiratory rate, gives
patients a distracting maneuver to perform when attacks
occur, and provides patients with a sense of self-control
during episodes of hyperventilation.
• This technique has been shown to be very effective in a
high proportion of patients with HVS.

How to Do It?
• Calm breathing involves taking
smooth, slow, and regular breaths.
• Sitting upright is usually better than
lying down or slouching, because it
can increase the capacity of your
lungs to fill with air.
• It is best to 'take the weight' off
your shoulders by supporting your
arms on the side-arms of a chair, or
on your lap.

How to Do It ?
1. Take a slow breath in through the nose, breathing into
your lower belly (for about 4 seconds)
2. Hold your breath for 1 or 2 seconds
3. Exhale slowly through the mouth (for about 4 seconds)
4. Wait a few seconds before taking another breath
• About 6-8 breathing cycles per minute is often helpful to
decrease anxiety, but find your own comfortable
breathing rhythm.
• These cycles regulate the amount of oxygen you take in
so that you do not experience the fainting, tingling, and
giddy sensations that are sometimes associated with
overbreathing.

• Benzodiazepines are useful in the treatment of hyperventilation
resulting from anxiety and panic attacks.
• Lorazepam (ativan) is a sedative-hypnotic of the benzodiazepine
class that has a short time to onset of effect and a relatively long
half-life.
• Diazepam (valium) depresses all levels of the CNS (eg, limbic and
reticular formation), possibly by increasing the activity of GABA.
It is considered second-line therapy for seizures.
• Paroxetine (paxil) is the alternative drug of choice for HVS. It is a
potent selective inhibitor of neuronal reuptake of serotonin and
has a weak effect on neuronal reuptake of norepinephrine and
dopamine.

Definitions
Asthma
Asthma is a heterogeneous disease, usually characterized by chronic airway
inflammation. It is defined by the history of respiratory symptoms such as wheeze,
shortness of breath, chest tightness and cough that vary over time and in intensity,
together with variable expiratory airflow limitation. [GINA 2014]
COPD
COPD is a common preventable and treatable disease, characterized by persistent
airflow limitation that is usually progressive and associated with enhanced chronic
inflammatory responses in the airways and the lungs to noxious particles or gases.
Exacerbations and comorbidities contribute to the overall severity in individual
patients. [GOLD 2015]
Asthma-COPD overlap syndrome (ACOS) [a description]
Asthma-COPD overlap syndrome (ACOS) is characterized by persistent airflow
limitation with several features usually associated with asthma and several features
usually associated with COPD. ACOS is therefore identified by the features that it
shares with both asthma and COPD.
GINA 2014, Box 5-1

Usual features of asthma, COPD and
ACOS
GINA 2014, Box 5-2A (1/3)
Feature Asthma COPD ACOS
Pattern of
respiratory
symptoms
Symptoms vary over time
(day to day, or over longer
period), often limiting
activity. Often triggered by
exercise, emotions
including laughter, dust, or
exposure to allergens
Chronic usually continuous
symptoms, particularly
during exercise, with ‘better’
and ‘worse’ days
Respiratory symptoms
including exertional dyspnea
are persistent, but variability
may be prominent
Lung function Current and/or historical
variable airflow limitation,
e.g. BD reversibility, AHR
FEV1 may be improved by
therapy, but post-BD
FEV1/FVC <0.7 persists
-
Airflow limitation not fully
reversible, but often with
current or historical
variability
Lung function
between
symptoms
May be normal Persistent airflow limitation Persistent airflow limitation
Age of onset Usually childhood but can
commence at any age
Usually >40 years Usually ≥40 years, but may
have had symptoms as
child/early adult

Usual features of asthma, COPD and
ACOS (continued)
Feature Asthma COPD ACOS
Past history or
family history
Many patients have
allergies and a personal
history of asthma in
childhood and/or family
history of asthma
History of exposure to
noxious particles or gases
(mainly tobacco smoking or
biomass fuels)
Frequently a history of
doctor-diagnosed asthma
(current or previous),
allergies, family history of
asthma, and/or a history of
noxious exposures
-
Time course Often improves
spontaneously or with
treatment, but may result in
fixed airflow limitation
Generally slowly progressive
over years despite treatment
Symptoms are partly but
significantly reduced by
treatment. Progression is
usual and treatment needs
are high.
Chest X-ray- Usually normal Severe hyperinflation and
other changes of COPD
Similar to COPD
Exacerbations Exacerbations occur, but
risk can be substantially
reduced by treatment
Exacerbations can be
reduced by treatment. If
present, comorbidities
contribute to impairment
Exacerbations may be more
common than in COPD but
are reduced by treatment.
Comorbidities can contribute
to impairment.
GINA 2014, Box 5-2A (2/3)

Syndromic diagnosis of airways disease
The shaded columns list features that, when present, best distinguish between
asthma and COPD.
For a patient, count the number of check boxes in each column.
 If 3 or more boxes are checked for either asthma or COPD, that diagnosis is
suggested.
 If there are similar numbers of checked boxes in each column, the diagnosis
of ACOS should be considered.

Differentiating COPD from asthma
• CommonClinical features COPD Asthma
Smoker or ex-smoker Nearly all Possibly
Symptoms under age 35 Rare Often
Chronic productive cough Common Uncommon
Breathlessness Persistent and
progressive
Variable
Night time waking with breathlessness and
or wheeze
Uncommon Common
Significant diurnal or day to day variability of
symptoms
uncommon Common

Potential Discharge
• In all patients who received nebulised β2
agonists
• Prior to presentation, consider an extended
observation period prior to discharge
• ƒIf PEF<50% on presentation, give prednisolone
40-50 mg/day for 5 days
ƒ

• In all patients ensure treatment supply of inhaled
steroid and β2 agonist and check inhaler technique
• ƒArrange follow up 2 days post-discharge
ƒ
• ƒRefer to chest clinic
Society, pp.116

• Corticosteroids are
recommended for most
patients in the emergency
department, especially:
• Those who do not respond
completely to initial SABA
therapy,
• Those whose exacerbation
develops even though they
were already taking oral
corticosteroids
• Those with previous
exacerbations requiring oral
corticosteroids
Drugs2009; 69 (17): 2363-2391

• Corticosteroids
• Steroids reduce mortality,
relapses, subsequent hospital
admission and requirement for
β2 agonist therapy.
• The earlier they are given in the
acute attack the better the
outcome.
• It is not known if inhaled steroids
provide further benefit in
addition to systemic steroids.
• Inhaled steroids should however
be started, or continued as soon
as possible to commence the
chronic asthma management
plan
• British Guideline on the Management of Asthma
revised Jan 2012
• Magnesium Sulfate
• Studies report the safe use of
nebulized magnesium sulphate,
in a dose of 135 mg-1152 mg, in
combination with β2 agonists,
with a trend towards benefit in
hospital admission.
• A single dose of IV magnesium
sulphate is safe and may improve
lung function in patients with
acute severe asthma

• Anticholinergics
• Combining nebulized ipratropium
bromide with a nebulized β2 agonist
produces significantly greater
bronchodilation than a β2 agonist
alone, leading to a faster recovery
and shorter duration of admission.
• Anticholinergic treatment is not
necessary and may not be beneficial
in milder exacerbations of asthma or
after stabilization
• Heliox
• The use of heliox, (helium/oxygen
mixture in a ratio of 80:20 or 70:30),
either as a driving gas for nebulizers,
as a breathing gas, or for artificial
ventilation in adults with acute
asthma is not supported on the basis
of present evidence.
• British Guideline on the Management of Asthma revised
Jan 2012
• Leukotriene Receptor Antagonists
• There is insufficient evidence at
present to make a recommendation
about the use of leukotriene receptor
antagonists in the management of
acute asthma
• Antibiotics
• When an infection precipitates an
exacerbation of asthma it is likely to
be viral.
• The role of bacterial infection has
been overestimated.
• Routine prescription of antibiotics is
not indicated for acute asthma.

Diagnose COPD
Consider a diagnosis of COPD for people who are:
– over 35, and
– smokers or ex-smokers, and
– have any of these symptoms:
• - exertional breathlessness
• - chronic cough
• - regular sputum production,
- frequent winter ‘bronchitis’
- Wheeze
– And no clinical features of asthma
[2004]

Managing stable COPD: inhaled
therapies
SABA or SAMA as required*
Breathlessness and
exercise limitation
Exacerbations or
persistent
breathlessness
Persistent
exacerbations or
breathlessness
LABA LAMA
Discontinue SAMA
________
Offer LAMA in
preference to regular
SAMA four times a day
LABA + ICS in a
combination inhaler
________
Consider LABA +
LAMA if ICS declined
or not tolerated
LAMA
Discontinue SAMA
________
Offer LAMA in
preference to regular
SAMA four times a
day
FEV1 ≥ 50% FEV1 < 50%
LABA + ICS
in a combination
inhaler
________
Consider LABA +
LAMA if ICS declined
or not tolerated
LAMA + LABA + ICS
in a combination inhaler
Offer Consider
* SABAs (as required) may
continue at all stages

Assess symptoms
Assess degree of airflow limitation using spirometry
Assess risk of exacerbations
Assess comorbidities
COPD Assessment Test (CAT)
or
Clinical COPD Questionnaire (CCQ)
or
mMRC Breathlessness scale
Assessment of COPD

COPD Assessment Test (CAT): An 8-item measure of health status impairment
in COPD
Clinical COPD Questionnaire (CCQ): Self-administered questionnaire developed
to measure clinical control in patients with COPD
Modified British Medical Research Council (mMRC) Questionnaire:
Breathlessness Measurement, relates well to other measures of health status and
predicts future mortality risk.
Assessment of Symptoms

Modified MRC (mMRC)Questionnaire
mMRC Grade Symptoms
Grade 0. Breathless with strenuous exercise.
Grade 1. Breathless when hurrying on the level or walking up a slight hill.
Grade 2. Breathless when walking on own pace on the level.
Grade 3. Breathless after walking about 100 meters on the level.
Grade 4. Breathless with minimal exertion

Classification of Severity of Airflow
Limitation in COPD*
In patients with FEV1/FVC < 0.70:
GOLD 1: Mild FEV1 > 80% predicted
GOLD 2: Moderate 50% < FEV1 < 80% predicted
GOLD 3: Severe 30% < FEV1 < 50% predicted
GOLD 4: Very Severe FEV1 < 30% predicted
*Based on Post-Bronchodilator FEV1

Patient Characteristic Spirometric
Classification
Exacerbations
per year
CAT mMRC
A
Low Risk
Less Symptoms
GOLD 1-2 ≤ 1 < 10 0-1
B
Low Risk
More Symptoms
GOLD 1-2 ≤ 1 > 10 > 2
C
High Risk
Less Symptoms
GOLD 3-4 > 2 < 10 0-1
D
High Risk
More Symptoms
GOLD 3-4 > 2 > 10
> 2
Global Strategy for Diagnosis, Management and
Prevention of COPD
Combined Assessment of
COPD
When assessing risk, choose the highest risk
according to GOLD grade or exacerbation
history. One or more hospitalizations for COPD
exacerbations should be considered high risk.)

Managing stable COPD: Oral
corticosteroids
• Maintenance use of oral corticosteroid therapy in COPD is not
recommended
• Some patients with advanced COPD may require maintenance oral
corticosteroids when these cannot be withdrawn following an
exacerbation
• The does of oral corticosteroids should be kept as low as possible
• Any patient treated with long term corticosteroid therapy should be
monitored for the development of osteoporosis and given appropriate
prophylaxis. Patients over the age of 65 should be started on prophylactic
treatment without the need for monitoring

Managing stable COPD: Oxygen
• Clinicians should be aware that inappropriate oxygen therapy in
• people with COPD may cause respiratory depression
• Use appropriate oxygen therapy:
• Long-term oxygen therapy
• Ambulatory
• Short burst

Managing stable COPD:
Cor pulmonale
• A diagnosis of cor pulmonale should be considered if patients have:
• - Peripheral odema, raised venous pressure, systolic parasternal
heave, a loud pulmonary second heart sound.
• Assess need for oxygen
• Use diuretics
• [2004]

Manage Stable COPD: Non-pharmacologic
Patient
Group
Essential Recommended Depending on local
guidelines
A
Smoking cessation (can
include pharmacologic
treatment)
Physical activity
Flu vaccination
Pneumococcal
vaccination
B, C, D
Smoking cessation (can
include pharmacologic
treatment)
Pulmonary rehabilitation
Physical activity
Flu vaccination
Pneumococcal
vaccination

Manage Stable COPD: Pharmacologic Therapy
(Medications in each box are mentioned in alphabetical order, and therefore not
necessarily in order of preference.)
Patient RecommendedFirs
t choice
Alternative choice Other Possible
Treatments
A
SAMA prn
or
SABA prn
LAMA
or
LABA
or
SABA and SAMA
Theophylline
B
LAMA
or
LABA
LAMA and LABA
SABA and/or SAMA
Theophylline
C
ICS + LABA
or
LAMA
LAMA and LABA or
LAMA and PDE4-inh. or
LABA and PDE4-inh.
SABA and/or SAMA
Theophylline
D
ICS + LABA
and/or
LAMA
ICS + LABA and LAMA or
ICS+LABA and PDE4-inh. or
LAMA and LABA or
LAMA and PDE4-inh.
Carbocysteine
N-acetylcysteine
SABA and/or SAMA
Theophylline

Arterial blood gas measurements (in hospital): PaO2 < 8.0 kPa
with or without PaCO2 > 6.7 kPa when breathing room air
indicates respiratory failure.
Chest radiographs: useful to exclude alternative diagnoses.
ECG: may aid in the diagnosis of coexisting cardiac problems.
Whole blood count: identify polycythemia, anemia or bleeding.
Purulent sputum during an exacerbation: indication to begin
empirical antibiotic treatment.
Biochemical tests: detect electrolyte disturbances, diabetes, and
poor nutrition.
Spirometric tests: not recommended during an exacerbation.
Manage Exacerbations: Assessments

• Antibiotics should be
given to patients with:
 Three cardinal
symptoms: increased
dyspnea, increased
sputum volume, and
increased sputum
purulence.
 Who require
mechanical ventilation.
Noninvasive ventilation (NIV)
for patients hospitalized for
acute exacerbations of COPD:
 Improves respiratory
acidosis, decreases
respiratory rate, severity of
dyspnea, complications and
length of hospital stay.
 Decreases mortality and
needs for intubation.

Therapeutic Options: COPD Medications
Beta2-agonists
Short-acting beta2-agonists
Long-acting beta2-agonists
Anticholinergics
Short-acting anticholinergics
Long-acting anticholinergics
Combination short-acting beta2-agonists + anticholinergic in one inhaler
Combination long-acting beta2-agonist + anticholinergic in one inhaler
Methylxanthines
Inhaled corticosteroids
Combination long-acting beta2-agonists + corticosteroids in one inhaler
Systemic corticosteroids
Phosphodiesterase-4 inhibitors

Lobar pneumonia
• Lobar pneumonia is acute bacterial
infection of a part of lobe the entire lobe,
or even two lobes of one or both the
lungs.
Pneumonia 121

Bronchopneumonia
• Bronchopneumonia is infection of the
terminal bronchioles that extends into the
surrounding alveoli resulting in patchy
consolidation of the lung.
Pneumonia 122

Community Acquired Pneumonia
(CAP)
Pneumonia which develops in an otherwise
healthy person outside of hospital or have
been in hospital for less than 48hrs
Pneumonia 123

Nosocomial pneumonia
(HAP)
Pneumonia that was not incubating upon
admission developing in a patient hospitalized
for greater than 48 hrs.
Pneumonia 124

Clinical Manifestations
• Indolent to fulminant in presentation
• Mild to fatal in severity
• Typical symptoms –
• Fever
• Chills
• Cough
• Rust coloured sputum
• Mucopurulent sputum
• Dyspnea ( shortness of breath)
• Pleuritic chest pain
• Elevated WBC
• Bacteraemic
Pneumonia 125

Antibiotic doses for treating pneumonia
Pneumonia 126

Treatment for special cases
1. Patient less than 60 years & without
comorbidities:-
Azithromycine ( 500mg OD) *1day
( 250mg OD) *4days
Norfloxacin/Levofloxacin (400mg OD) *7days
2. Outpatient greater than 65 years:-
Norfloxacin (400mg OD) *7days or
Ceftriaxon (1-2 g/day) / Cifixim (2-4 g/day) 3rd gen
cefalosporins +
Pneumonia 127

Macrolides like Azithromycin ( 500mg OD) *1day
( 250mg OD) *4days
3. Patient is hospitalised but not severely ill:-
Combination of 3rd gen cefalosporins + Macrolides
Ceftriaxone + Azithromycin
OR
Norfloxacin/Levofloxacin (400mg OD)
4. If the patient is hospitalised but not severely ill:-
Combination of 3rd gen cefalosporins + Macrolides
and newer fluroquinolones (Gatifloxacin)
Pneumonia 128

5. Patient hospitalised & severely ill:-
Combination of 3rd gen cefalosporins +
Macrolides
and newer fluroquinolones
(Gatifloxacin)
We can add Vancomycin.
6. Patient with icu admission:-
3rd gen cefalosporins + Fluroquinolones
(Gatifloxacin)
+
Nutritional supplements + Saline
Vancomycin/Meropenam
Pneumonia 129

7. For HAP:-
Cephalosporins + Aminoglycocides
8. For antipseudomons cephalosporins:-
Ceftazidime + Cefexime
Pneumonia 130

Drugs with usual doses
Pneumonia 131

SIGN AND SYMPTOMS OF ACUTE LVF

Definition of Heart Failure
Classification Ejection
Fraction
Description
I. Heart Failure with
Reduced Ejection Fraction
(HFrEF)
≤40% Also referred to as systolic HF. Randomized clinical trials have mainly
enrolled patients with HFrEF and it is only in these patients that
efficacious therapies have been demonstrated to date.
II. Heart Failure with
Preserved Ejection Fraction
(HFpEF)
≥50% Also referred to as diastolic HF. Several different criteria have been used
to further define HFpEF. The diagnosis of HFpEF is challenging because
it is largely one of excluding other potential noncardiac causes of
symptoms suggestive of HF. To date, efficacious therapies have not been
identified.
a. HFpEF, Borderline 41% to 49% These patients fall into a borderline or intermediate group. Their
characteristics, treatment patterns, and outcomes appear similar to those
of patient with HFpEF.
b. HFpEF, Improved >40% It has been recognized that a subset of patients with HFpEF previously
had HFrEF. These patients with improvement or recovery in EF may be
clinically distinct from those with persistently preserved or reduced EF.
Further research is needed to better characterize these patients.

AHF with distinct clinical conditions

Goals of treatment in acute heart failure

Algorithm for management of acute pulmonary
oedema/congestion

Drugs Commonly Used for HFrEF
(Stage C HF)
Drug Initial Daily Dose(s) Maximum Doses(s)
Mean Doses Achieved in
Clinical Trials
ACE Inhibitors
Captopril 6.25 mg 3 times 50 mg 3 times 122.7 mg/d (421)
Enalapril 2.5 mg twice 10 to 20 mg twice 16.6 mg/d (412)
Fosinopril 5 to 10 mg once 40 mg once ---------
Lisinopril 2.5 to 5 mg once 20 to 40 mg once 32.5 to 35.0 mg/d (444)
Perindopril 2 mg once 8 to 16 mg once ---------
Quinapril 5 mg twice 20 mg twice ---------
Ramipril 1.25 to 2.5 mg once 10 mg once ---------
Trandolapril 1 mg once 4 mg once ---------
ARBs
Candesartan 4 to 8 mg once 32 mg once 24 mg/d (419)
Losartan 25 to 50 mg once 50 to 150 mg once 129 mg/d (420)
Valsartan 20 to 40 mg twice 160 mg twice 254 mg/d (109)
Aldosterone Antagonists
Spironolactone 12.5 to 25 mg once 25 mg once or twice 26 mg/d (424)
Eplerenone 25 mg once 50 mg once 42.6 mg/d (445)

Drugs Commonly Used for HFrEF
(Stage C HF) (cont.)
Drug Initial Daily Dose(s) Maximum Doses(s)
Mean Doses Achieved in Clinical
Trials
Beta Blockers
Bisoprolol 1.25 mg once 10 mg once 8.6 mg/d (118)
Carvedilol 3.125 mg twice 50 mg twice 37 mg/d (446)
Carvedilol CR 10 mg once 80 mg once ---------
Metoprolol succinate
extended release
(metoprolol CR/XL)
12.5 to 25 mg once 200 mg once 159 mg/d (447)
Hydralazine & Isosorbide Dinitrate
Fixed dose combination
(423)
37.5 mg hydralazine/
20 mg isosorbide dinitrate
3 times daily
75 mg hydralazine/
40 mg isosorbide
dinitrate 3 times daily
~175 mg hydralazine/90 mg
isosorbide dinitrate daily
Hydralazine and isosorbide
dinitrate (448)
Hydralazine: 25 to 50 mg,
3 or 4 times daily and
isorsorbide dinitrate:
20 to 30 mg
3 or 4 times daily
Hydralazine: 300 mg
daily in divided doses
and isosorbide dinitrate
120 mg daily in divided
doses
---------

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