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Presented by:

1) Muhamad Yusof
2) Shazwani
3) Norhana
4) Khairunnisa Zafirah
5) Nur Ashila
6) Nor Amalina
Case 1
1) A 72-year old man presented with a complaint of
worsening exertional dyspnea for several weeks.
• He feels short of breath after walking 100 feet.
• No chest pain
• He had felt lightheaded, nearly faint while climbing a flight
of stairs, but relieved when he sat down.
• Difficulty sleeping at night and has to prop himself up with
2 pillows.
• Occasionally, he wakes up at night feeling quite short of
breath, which is relieved within minutes by sitting upright.
• He denies any significant medical history,
• Not on regular medications, doesn’t smoke or drink alcohol.
DIFFERENTIAL DIAGNOSIS
Congestive Heart Failure
Pros:
- worsening exertional dyspnea
- Orthopnea
- Nocturnal episode of severe paroxymal
dyspnea
Myocardial Infarction
Pros:
- worsening exertional dyspnea
- nearly faint
Cons:
- severe chest pain
Cont…..
Emphysema
Pros:
- Worsening exertional dyspnea progressing to
dyspnea at rest
Cons:
- Progressing for many years

Pulmonary Vascular Occlusive Diseases (eg.


Pumonary Embolism)
Pros:
- Near syncope on exertion
Cons:
- Repeated episodes of dyspnea at rest (recurrent
pulmonary embolism)
CARDIOVASCULAR CAUSES OF

DYSPNEA Acute left heart failure cause acute pulmonary edema

• Increase central venous pressure

• Increase pulmonary venous and capillary pressure

• Hydrostatic pressure of pulmonary capillaries > oncotic pressure of plasma


( 25-30mmHg )

• Fluids moves into interstitium and alveoli cause pulmonary congestion and edema

• Reduce lung compliance, lead to hypoxaemia

• Dyspnea
Myocardial ischaemia

 Induce true breathlessness by provoking


transient left ventricular dysfunction or heart
failure

transient left ventricular dysfunction

increase left ventricular diastolic pressure

Increase pulmonary congestion

Hypoxeamia & Dyspnea


INVESTIGATIONS
These tests may be helpful in determining
whether dyspnea is produced by heart
disease, lung disease, abnormalities of
the chest wall, or anxiety:
Echocardiography or radionuclide
ventriculography
Pulmonary function testing
exercise treadmill test
MANAGEMENT
Urgent treatment:
i. Sit the patient
ii. Give oxygen
iii. Administer nitrates
iv. Administer a loop diuretic like
furosemide
Clinical Scenario
A 65-years-old man with a long
history of smoking and alcohol
intake, present to the emergency
department with a 4 days history of
fever, cough that is productive of
thick, foul smelling sputum
,dyspnoea for 3 days at rest, and left
pleuritic chest pain.
DIFFERENTIAL
DIAGNOSIS???
Differential diagnosis:-
• Pneumonia
• Chronic bronchitis
• Bronchial asthma
• Pulmonary embolism
• Congestive heart failure
Physical examination
On examination, he has a
temperature of 38.8. He has dullness
to percussion over the posterior left
lower lung zone; bronchial breath
sounds and crackles are noted over
the same area.
Condition History Signs

Massive •Prolong bed rest or •Severe central cyanosis


pulmonary other risk factor •Elevated JVP
embolus •Severe central chest •Shock (tachycardia, reduce BP)
pain
•Previous pleurisy
•Syncope
•Dizziness
•Immediate dyspnea

Acute •History of previous •Tachycardia


severe episodes. •Cyanosis (late)
asthma •Family history of •Peak flow meter reading ↓
asthma •Rhonci
•Asthma medications •Chest wall movement ↓at both
•Wheeze side
•Immediate dyspnea •Normal perccussion and vocal
resonance
COPD •Previous episodes •Signs of COPD(expiratory
of breathlessness wheezing, barrel chest,use
and productive accessory muscle)
cough •Emphysema referred to as
•Weeks to year “pink puffers
dyspnea. •Chronic bronchitis are
classically labeled “blue
bloaters
•Chest wall movement ↓both
side

Pneumonia •Fever
•Fever •Pleural rub
•Rigors •Cyanosis (severe case)
•Pleuritis •Reduced chest wall movement
•Hours to day at effected side
dyspnea •Dullness on percussion at
effected site
•Bronchial breath sound
Congestive heart •Dyspnea on exertion •JVP distension
failure •Orthopnea •hepatomegaly
• Nocturnal episode of •Tachycardia and
severe paroxymal tacypnea
dyspnea •Displaced apex beat
Pathophysiology of
pneumonia
Infection

Proliferation of microorganisms within the alveolar space

Acute inflammatory response

Increase alveolar capillary permeability

Impaired ventilation

Decreased lung compliance

Increased the work of breathing

Dyspnoea
Pathophysiology of COPD
Loss
Inflammation and Mucus
elasticity and
scarring of small secretion
alveolar
airway
attachment
Block airway
Reduce elastic
recoil

Airway
collapse
during
expiration
Narrowing of
small airway
and air
trapping
Hyperinflation of
lung and
breathlessness
Investigation
• Chest X-Ray
• Electrocardiogram
• Arterial Blood Gases
• Full blood count
• Sputum and blood culture
• Echocardiogram
Principles of management
Treatment of pulmonary infection
• Antibiotic
Treatment of airway obstruction
• Bronchodilator
Pleuritic pain
• Analgesia
Hypoxaemia
• Oxygen
Others
• Vaccination, diuretics for oedema, exercise training to
improve sense of wellbeing and breathlessness
Clinical Scenarios
• SYAHID, 14 year old boy presents to
ED complaining of severe shortness
of breath. He has long standing
poorly controlled, Diabetes Mellitus
type 1 for the past 6 years
• About 3 days before admission, he
had several episodes of vomiting, 5
times per day.
• Associated with generalize severe sudden
burning abdominal pain 1 days prior to
admission
• Since then he has noted progressive SOB.
Initially the SOB only occur on minimal
exertion.
• He also complain of passing massive
volume of urine ,drinking so much of
water per day, feel tired every day
• He had history of coma before
• He is on regular insulin
supplement since 6 years ago
• Both Parent have history of diabetes
mellitus
On examinations:
Patient look very thin, fast breathing, obvious
sub costal resection
• BP = 100/75 mmHg, RR = 32/min, O2
saturation = 88%.
• Pulse rate =95/ min
• Capillary refill time = 3 second
• Impression = tachypnoe, dehydration
• Provisional diagnosis?
• Differential diagnosis?
• What investigations that you would
like to do?
Come with shortness of breath
??? Why???
Differential diagnosis?
• Asthma
• Bronchitis
• Diabetic ketoacidosis
• Chronic obstructive pulmonary disease
• pulmonary edema
• Pulmonary embolism
Diabetic ketoacidosis

• Diabetic ketoacidosis (DKA)


is a potentially life-threatening
complication in patients with
diabetes mellitus.
• It happens predominantly in
those with type 1 diabetes,
Cause

• who already have diabetes


• inadequate insulin administration
• diabetes mellitus type 1
• diabetes mellitus type 2
• eating disorder
Symptoms of Diabetic
ketoacidosis
• nausea and vomiting
• increased respiratory rate.
• Shortness of breath
• dry mouth
• abdominal pain
• decrease in the level of
consciousness
• lethargy
How ketoacidosis cause
dyspnea???
• In ketoacidosis pH is low and acidic
so cause
• The body buffers this with a
mechanisms to compensate for the
acidosis,
• such as hyperventilation to lower
the blood carbon dioxide levels.
This hyperventilation cos dyspnea
• , in its extreme form, may be
observed as Kussmaul respiration.
• deep and labored breathing pattern
associated with severe metabolic
acidosis, particularly diabetic
ketoacidosis (DKA) but also renal
failure.
• Oooo….so the acidosis associate with
occumulation of co2,,so body try to
lower partial pressure of co2 by
increase respiration ..then cause
dyspnea..
investigation
• plasma glucose …glucose level
• Urea and electrolyte ….na usually increase
• Blood culture..infection by what?
• FBC…infection??
• Urine test.. keturia, glycosuria,
• Chest x ray…lung normal???
• Renal function test….cross react with
keton?
Management
• Monitor vital sign
• Monitor glucose level..insulin supplement
• Fluid replacement to correct dehydration
• Ventilation support,o2
• Antibiotic …if infection
• Iv bicarbonate
• Recheck atrial pH
DYSPNOEA
DEFINITIONS:
feeling of uncomfortable
need to breath

INSATIABLE
RESPIRATORY
DISTRESS DESPITE
MAXIMAL EFFORTS
TO BREATHE
Dyspnoea occurs whenever
the work of breathing is
excessive
Mechanisms of
DYSPNOEA
Dyspnea is characterized by an excessive or
abnormal activation of the respiratory
centers in the brainstem
STIMULI:-

(1) Intrathoracic receptors via the vagal nerves;


(pneumothorax, intestitial inflammation, pul.
Embolus)
(2) Afferent somatic nerves,particularly from the
respiratory muscles and chest wall, but also from
other skeletal muscles and joints;
(increased mech. load on ms.-obstruction, pul.
Fibrosis )
(3) Chemoreceptors in the brain, aortic, and carotid
bodies, and elsewhere in the circulation;
(HYPOXIA, HYPERCAPNIA OR ACIDOSIS)
(4) Higher (cortical) centers;
(5) Afferent fibers in the phrenic nerves

harrison’s text book


harrison’s text book
Dyspnoea may present either with
• Chronic dyspnoea on exertion or
• Acute dyspnoea at rest
Some causes of dyspnoea
System Acute dyspnea at rest Chronic exertional
dyspnea
CVS *Acute pulmonary Chronic heart failure
edema Myocardial ischemia
RS *Acute severe asthma *COPD
*Acute on COPD *Chronic asthma
*Pneumothorax Bronchial carcinoma
*Pulmonary Embolus Intestitial lung disease
ARDS Chronic pulmonary
Inhale foreign body thromboembolism
Lobar collapse Lymphatic
carcinomatosis
Laryngeal edema
Large pleural effusion

others Metabolic acidosis Severe anemia


Psychogenic obesity
hyperventilation
Types
• Nocturnal dyspnoea
• Orthopnoea
• Trepopnoea
• platypnoea
Grades (NYHA)
• 1- while doing more than normal activity
• 2- regular activity (moderate exercise)
• 3- mild exertion ( household work)
• 4- at rest.
• How to diagnose?????
Diagnosis: History
• Pulmonary embolus suggested by sudden onset
of shortness of breath or chest pain
• COPD exacerbation suggested by history of
Heavy smoking, cough, sputum production
• Cardiogenic pulmonary edema suggested by
chest pain, paroxysmal nocturnal dyspnea, and
orthopnea
Diagnosis: Physical Findings
1. Wheezing suggests airway obstruction:
– Bronchospasm
– Fixed upper or lower airway pathology
– Secretions
– Pulmonary edema

2. Stridor suggests upper airway obstruction


3. Elevated jugular venous pressure suggests right ventricular
dysfunction due to accompanying pulmonary hypertension
4. Tachycardia and arrhythmias may be the cause
• of cardiogenic pulmonary edema
Diagnosis: Laboratory Workup
ABG
• Quantifies magnitude of gas exchange
abnormality
Complete blood count
• Anemia
• Polycythemia suggests may chronic hypoxemia
• Leukocytosis, a left shift, or leukopenia
suggestive of
• infection
Cardiac serologic markers
• Troponin, Creatine kinase- MB fraction
(CK- MB)
Microbiology
• Respiratory cultures: sputum/tracheal
• aspirate/broncheoalveolar lavage (BAL)
• Blood, urine and body fluid (e.g. pleural)
cultures
Diagnostic Investigations

Chest radiography
• Identify chest wall, pleural and lung parenchymal
pathology; and distinguish disorders that cause
primarily V/Q mismatch (clear lungs) vs. Shunt
(intra- pulmonary shunt; with opacities present)
Electrocardiogram
• Identify arrhythmias, ischemia, ventricular
dysfunction
Echocardiography
• Identify right and/or left ventricular dysfunction
RESPIRATORY FAILURE

Definition
Classification
Etiology
Management
Monitoring
Components of respiratory
system
• CNS (Brain stem, spinal cord)
• Neuromuscular
• Airway
• Lung parenchyma (alveolar-capillary unit)
• Pulmonary circulation
• Chest wall (pleura, respiratory muscle, bones)

* Defect in each of these components may result in respiratory failure.


Definition

• A syndrome of inadequate pulmonary gas


exchange which leads to hypoxia with or
without hypercarbia due to dysfunction of
any component of the resp system.

• PaO2 < 8 kPa (60mmHg).


• PaCO2 > 7 kPa (55 mmHg).
Classification

• Type 1
• Acute hypoxic
• O2↓, CO2 normal or low
• Due to condition that affect/damage lung tissue

• Type 2
• Ventilatory failure
• O2↓, CO2↑
• Alveolar hypoventilation (decreased alveolar minute
ventilation)- fail to remove CO2
• Type 3
• Due to lung atelectasis in perioperative period.
• After GA, functional residual capacity decreases and lead to
collapse of dependent lung units.
• A.k.a. Perioperative respiratory failure

• Type 4
• Due to hypoperfusion of respiratory muscles in patients
who are in shock.
Etiology
Impaired
component: lung
tissue & pulm.
circulation.
• Type 1:
– Pneumonia
– Pulmonary edema
• Cardiogenic e.g. LVF
• Non-cardiogenic e.g. ARDS, ALI
– Pulmonary embolism
– Pulmonary fibrosis
– Atelectasis
• Type 2: Impaired components:
CNS, airway, n/muscular
– Central hypoventilation: transmission, chest wall.
• Drug overdose
• Brainstem injury
• Hypothyroidism
– Airway: Asthma, COPD
– Impaired neuromuscular transmission:
• Myasthenia Gravis
• Guillain-Barre Syndrome
• Phrenic nerve injury
– Resp. muscle weakness: Myopathy, hypophospathemia
– Chest wall deformity: kyphoscoliosis
– Pleura: Pneumo/hydro/haemothorax
– Morbid obesity ( Obesity Hypoventilation Syndrome)
• Type 3:
– Inadequate post-op anelgesia, upper
abdominal incision (attemp to ↓ intra-
abdominal pressure)
– Pre-op tobacco smoking
– Obesity, ascites
– Excessive airway secretions

• Type 4
– Cardiogenic/ septic/ hypovolemic shock.
Outline of Management
• Treat underlying cause(s):
• Infection: antibiotics
• Airway obstruction: bronchodilator, corticosteroids
• Improve cardiac function: diuretics, vasodilator, inotropy.

• Oxygen therapy via simple face mask or nasal canulla.


(O2 conc. 35-55%; O2 flow rate 6-10L/min.)

if not improve/ PaCO2 ↑, need urgent

• Respiratory support (Mechanical ventilation):


• Non-invasive - via tight-fitting nasal or face mask.
• Invasive - need endotracheal intubation/ tracheostomy.
Monitoring of Respiratory
Failure
• Clinical assessment of respiratory distress
– signs:
• Use if accessory muscle
• Intercostal recession
• Tachypnoea, tachycardia, sweating
• Unable to speak, unwillingness to lie flat
• Restlessness, reduced conscious level

• Pulse oximetry- measure the arterial O2 saturation (SaO2)


• Blood gas analysis
• Capnography – analysis of expired CO2 conc.

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