This presentation covers these related topics.

1. DYSPNEA, RESPIRATORY FAILURE, PNA
(PNEUMONIA), DAH ( DIFFUSE ALVEOLAR
HEMORRHAGE), PE (PULMONARY EMBOLISM)
BY NAKIGANDA ANGELLA N.,
TOOLIT GIVEN,
SENGOOBA DENNIS NYANZI

2. OUTLINE FOR EACH
● Causes
● Presentation
● Investigations
● Mgt

3. RESPIRATORY FAILURE
It occurs when pulmonary gaseous exchange fails to
maintain normal arterial oxygen and carbon dioxide
levels
There are two types I and II which are defined by the
absence or presence of hypercapnia(increased partial
pressures of carbon dioxide)

4. TYPE 1(HYPOXEMIC) RESPIRATORY FAILURE
Defined as a low level of oxygen in blood(hypoxemia)or (Pa02 <60 mm Hg)without an increased level of
carbon dioxide (the partial pressures of CO2 maybe normal or low) hypoxemia without hypercapnia
It’s mainly caused by a ventilation perfusion mismatch ie volume of air flowing in and out of the lungs is
not matched with the flow of blood to the lungs
It’s caused by conditions that affect oxygenation
● Low ambient oxygen like in high altitudes.
● V/Q mismatch from pulmonary embolism,Alveolar hypo-ventilation in acute neuromuscular diseas
● Shunts (atrio-septal defects)
● Diffuse problem from pneumonia and acute respiratory distress syndrome

5. TYPE II RESPIRATORY FAILURE
Defined as the buildup of carbon dioxide levels in the body due to failure of expulsion. PaCO2 >50
mmHg, hypoxemia with hypercapnia
It’s caused by
● inadequate alveolar ventilation from drug overdose,brain stem lesion,extreme obesity.
● Neuromuscular problems like Guillian Barre syndrome,motor neuron diseases
● Chestwall abnormalities like kyphoscoliosis,ankylosing spondylitis or flail chest.
● Increased airway resistance like COPD,asthma,suffocation.

6. …
● .

7. PATHOPHYSIOLOGY
 When disease impairs ventilation of part of a lung,perfusion of that region results in hypoxic and
carbon dioxide laden (deoxygenated) blood to enter the pulmonary veins
 The neighboring regions(which are still normal) eventually increase their ventilation thus accelerate the
excretion of the accumulation carbon dioxide in the pulm.veins
 This corrects the arterial carbon dioxide to normal but can’t augment oxygen uptake because the
hemoglobin flowing through the normal regions is already saturated
 Mixture of blood from the underventilated and normal regions results in hypoxia with normocapnia
(normal partial pressures of carbon dioxide ). This is type I respiratory failure
 Arterial hypoxia with hypercapnia( increased partial pressures of carbon dioxide)results into Type II
respiratory failure

8. CLINICAL PRESENTATION
Pulmonary findings- pulmonary edema,asthma,COPD,pneumonia
Neurological manifestations-restlessness,confusion,seizures or coma
Asterixis(type II)
Tachycardia and arrhythmias from hypoxemia and acidosis
Peripheral and central cyanosis
Dyspnea-uncomfortable sensation of breathing
Pulmonary hypertension ( from pulmonary arteriolar constriction caused by alveolar hypoxemia
potentiated by hypercapnia)

9. INVESTIGATIONS
• Do full medical history and physical exam
• Pulse oximetry test for oxygen saturation rate
• Pulmonary function tests
• Arterial blood gas test I.e CBC (to establish severity of
hypoxemia,hypercapnia,acidemia,bicarbonate or polycythemia
• LFTs and RFTs to provide etiology of the respiratory failure
• Imaging tests like Chest X-ray, CT scans.
• Echocardiogram to rule out any cardiovascular cause,detect dysrythmias
from severe hypoxemia or acidosis
• Serum electrolytes test because potassium,Magnesium and Phosphate
may aggravate respiratory failure
• Bronchoscopy.

10. MANAGEMENT OF ACUTE RESPIRATORY FAILURE
Prompt diagnosis and management of the underlying cause is important
In type 1, high concentrations of oxygen (40-60% by mask) will usually relive hypoxia by increasing
the alveolar P02. O2 for SPO2 <93% on room air
In severe cases, mechanical ventilation may be needed to relieve hypoxia. If high concentrations of
oxygen for more than a few hours should receive humidified oxygen
NB; No opioids because they suppress ventilatory drive

11. PULMONARY EMBOLISM (PE)
Definition - lodging of a blood clot in the pulmonary arterial tree with subsequent increase in
pulmonary vascular resistance, impaired V/Q matching, and possibly reduced pulmonary blood
flow

12. ETIOLOGY AND PATHOPHYSIOLOGY
• One of the most common causes of preventable death in the hospital
• Proximal leg thrombi (popliteal, femoral, or iliac veins) are the source of most clinically
recognized pulmonary emboli
• Thrombi often start in calf, but must propagate into proximal veins to create a sufficiently large
thrombus for a clinically significant PE. Fewer than 30% of patients have clinical evidence of DVT
(e.g. Leg swelling, pain, or tenderness)
• Suspect PE if patient develops fever, sudden dyspnea, chest pain, or collapse 1-2 wk after surgery

13. RISK FACTORS
.

14. FEATURES
● .

15. INVESTIGATIONS
.

16. MGT
• General Measures: Prompt recognition is life saving
• Provide sufficient oxygen to hypoxaemic patients so as to keep the SpO2 >90%
• Fluid resuscitation with intravenous fluids and volume expanders for patients with circulatory shock
• Avoid diuretics and vasodilators because they reduce the cardiac output
• Give opioids to relieve pain and distress but carefully used in hypotensive patients. External massage may be
good in moribund patients for it dislodges and breaks up the central embolus
• Give anticoagulation therapy eg. LMWH, UFH, DAOA
• Thrombolysis and surgical therapy-Thrombolysis is for patients with acute massive PE and cardiogenic shock
plus those with right ventricular dilatation and hypokinesis or severe hypoxia. Surgical pulmonary embolectomy
may be done for patients that may have high mortality
• Caval filters- for patients with severe hemorrhage on using anticoagulants or recurrent VTE. Retrievable filters
should be used in patients with temporary risk factors and used till patient is stable on anticoagulants.

17. DIFFUSE ALVEOLAR HEMORRHAGE
Diffuse alveolar hemorrhage is persistent or recurrent pulmonary hemorrhage.
Diffuse alveolar hemorrhage results from widespread damage to the pulmonary small vessels,
leading to blood collecting within the alveoli. If enough alveoli are affected, gas exchange is
disrupted. The specific pathophysiology and manifestations vary depending on cause.

18. ETIOLOGY
● Autoimmune disorders (Goodpasture syndrome, antiphospholipid antibody syndrome,
connective tissue disorders) MOST COMMON
● Pulmonary infections (eg, hantavirus infection, covid)
● Toxic exposures (eg,certain pesticides)
● Drug reactions (eg, amiodarone, methotrexate, nitrofurantoin
● Cardiac disorders (eg, mitral stenosis)
● Coagulation disorders caused by diseases or anticoagulant drugs
● Idiopathic pulmonary hemosiderosis
● Hematopoietic stem cell transplantation or solid organ transplantation

19. CONT’D
Features; Dyspnea,Cough, Features of anemia, Hemoptysis, Fever
Dx
● Chest x-ray ie features of diffuse bilateral alveolar infiltrates and a suspicion of diffuse
alveolar hemorrhage
● Bronchoalveolar lavage
● Serologic and other tests to diagnose the cause ie (antinuclear antibody, anti–double-
stranded DNA [anti-dsDNA], antiglomerular basement membrane [anti-GBM] antibodies,
antineutrophil cytoplasmic antibodies [ANCA], antiphospholipid antibody)

20. MGT
● Corticosteroids
● Sometimes cyclophosphamide, rituximab, or plasma exchange/plasmapheresis
● Supportive measures
Treatment involves correcting the cause.
Corticosteroids and possibly cyclophosphamide are used to treat vasculitides, connective tissue
disorders, and Goodpasture syndrome .
Cyclophosphamide- chemotherapeutic used to treat cancers and autoimmune diseases.

21. MGT ...
Plasma exchange may be used to treat Goodpasture syndrome.
Several studies have reported successful use of recombinant activated human factor VII in treating
severe unresponsive alveolar hemorrhage, but such therapy is controversial because of possible
thrombotic complications.
Other possible management measures include supplemental oxygen, bronchodilators, reversal of
any coagulopathy, and intubation with protective strategies as for acute respiratory distress
syndrome (ARDS) and mechanical ventilation .

22. PNEUMONIA
Acute infection and inflammation of the lungs alveoli.
There are two major types:
● Bronchopneumonia: involves both the lung parenchyma and the bronchi. Common in
children and the elderly
● Lobar pneumonia: involves one or more lobes of the lung. Common in young people
Causative agents can be viral, bacterial or parasitic.

23. CAUSES
Pathogens vary according to age, patient’s condition and whether infection was acquired in the
community or hospital (Gram negative are more common in hospital).
● Neonates: group B streptococcus, Klebsiella, E.coli, Chlamydia and S. aureus
● Children <5 years: Pneumococcus, Haemophilus influenzae, less frequently: S. aureus, M.
catarrhalis, M. Pneumoniae, viruses (RSV, influenza, measles)
● Adults and children >5 years: most commonly S.pneumoniae, followed by atypical bacteria,
e.g. Mycloplasma pneumoniae, viruses
● Immunosuppressed: Pneumocystis (in HIV infected)

24. PREDISPOSING FACTORS
● Malnutrition
● Old age
● Immunosuppression (HIV,
cancer, alcohol dependence)
● Measles, pertussis
● Pre existing lung or heart
diseases, diabetes

25. PRESENTATIONS
● Fever, chest pain, cough (with or without sputum), rapid breathing (> 30 bpm), chest
indrawing for children and severe cases
● If severe; Pulse >120/minute Temperature > 39.5 o C, Low BP < 90/60 mmHg, Oxygen
saturation less than 90
● Extrapulmonary features, e.g. confusion or disorientation, may predominate and may be the
only signs of pneumonia in elderly or immunosuppressed patients

26. INVESTIGATIONS
● Do a chest X-ray and look for complications, e.g. –
Pneumothorax, pyothorax – Pneumonitis suggestive of
pneumocystis jiroveci pneumonia (PCP) – Pneumatocoeles
(cavities filled with air) suggestive of staphylococcal
pneumonia
● Sputum: For Gram stain, Ziehl-Neelsen (ZN) stain, culture for
AFB
● Blood: Complete blood count

27. MGT
.

28. PNEUMOCYSTIS PNEUMONIA, PCP
● Interstitial pneumonitis caused by
the parasite/fungus
Pneumocystis jirovecii (formerly
carinii). It is common in severely
immunosuppressed patients (e.g.
in HIV).

29. ...
.

30. DYSPNEA
Definition.
Is a term general applied to sensations experienced by individuals who complain of unpleasant
or uncomfortable respiratory sensation or simply difficult, laboured, uncomfortable breathing
Or Sensation of feeling breathless or experiencing air hunger. Its It's a subjective sensation of
breathing that varies from mild discomfort to feeling of suffocation.

31. MECHANISM OF DYSPNEA.
Dyspnea occurs when there is a mismatch between afferent and efferent signalings.
As the brain receives afferent ventilation information, it is able to compare it to the current level
of respiration by the efferent signals.
If the level of respiration is inappropriate for the body status and need , the dyspnea occurs.

32. PATHOPHYSIOLOGY OF DYSPNEA.
There are many theories as regards dyspnea. however the most attractive unifying theory is that
dyspnea results from dissociation or a mismatch between central respiratory motor activity and
incoming afferent information from receptors in the airway, lungs and chest wall structures.
The afferent feed back from peripheral sensory receptors may allow the brain to assess the
effectiveness of the motor command issued to the ventilatory muscles I.e the appropriateness
of the response in terms of the flow and volume for the command.

33. ,,,
When changes in respiratory pressure, airflow , or movement of the lungs and chest wall are not
appropriate for outgoing command , the intensity of dyspnea is heightened
In other words, a dissociation between the motor command and the mechanical response of the
respiratory system may produce a sensation of respiratory discomfort.
When the motor signals are sent to chest wall from the respiratory centre, the sensory cortex is
simultaneously activated, resulting into conscious sensation of muscular effort and
breathlessness.
There is a strong psychological component to dyspnea, as some people may become aware of
their breathing in such circumstances but not experience the distress typical of the condition.

34. CAUSES OF DYSPNEA.
There are generally four categories.
1. Cardiac
○ Congestive cardiac failure
○ Coronary artery disease
○ Cardiomyopathy
○ Valvular dysfunction
○ Pericarditis
○ Arrhythmias
2. Pulmonary
○ COPD
○ Asthma
○ Restrictive lung disease
○ Pneumothorax.
3. Cardiac + pulmonary.
● COPD with pulmonary hypertension and
corpulmonale
● Chronic pulmonary emboli.
4. Non cardiac , non pulmonary causes.
● Metabolic conditions ( acidosis)
● Pain in the chest wall
● Neuro vascular disorders
● Otorhinolaryngeal disorder.

36. HISTORY ( ONSET AND CAUSE)
Ask about the onset and the cause of dyspnea to the client whether it's a chronic or acute issue
Acute causes ( within minutes)
Respiratory
● Acute exacerbation of asthma
● Pneumothorax
● Pulmonary embolism
● Foreign body
● Laryngeal oedema

37. SUB ACUTE CAUSES.
Within hours.
● Asthma
● Left heart failure
● Pneumonia.
Within days.
● Pneumonia
● ARDS
● Left heart failure.
Within weeks.
● Pleural effusion
● Anaemia
● Muscles weakness
● Tumours
Pleural =Effusion, Malignancy, Fibrosis
Parenchyma = Interstitial lung disease
Vascular = Vasculitis, A-V malformations.

38. HISTORY ( POSITION AT WHICH THE DYSPNEA OCCURS).
Orthopnea
Shortness of breath which occurs when lying flat , causing the person to have to sleep propped up in
bed or sitting in a chair.
Causes
● CCF
● Left ventricular heart failure
● COPD
● Bronchial asthma
● Massive pleural effusion
● Ascites
● GERD.

39. OTHERS
Platypnea - Shortness of breath that is relieved when lying down and worsens when sitting or
standing. Its It's the opposite of orthopnea
Causes
• Left atrial myxoma
• Massive pulmonary embolism
• Paralysis of intercostal muscles
• Hepato pulmonary symdrome .
Trepopnea - Shortness of breath that is sensed while lying on one side but not on the other ( lateral
recumbent position.
Common causes
• Diseases one lung or bronchi
• Congestive cardiac failure

40. HISTORY ( TIMING OF DYSPNEA)
1. Nocturnal onset dyspnea. Dyspnea that occurs mostly at night.
● Congestive cardiac failure
● COPD
● Bronchial asthma
● Sleep apnea
2. Severity of the nocturnal onset dyspnea, if its severe enough that awakens the person from sleep.
Making them sit or stand ( suspect underlying heart failure.
3. Post prandial dyspnea
● GERD
● Aspiration
● Food allergy.

41. GRADING OF THE DYSPNEA. ( HISTORY)
mMRC dyspnea scale. ( modified from medical research council for dyspnea scale)
Grade. Dyspnea related to activity.
0 Breathless only on strenuous exercise.
1. Breathless when hurrying on the level or walking up a slight hill.
2. Walks slower than other people of the same age on the same level due to shortness of
breath or need to stop for breath when walking on her own phase.
3. Shortness of breath after walking few minutes on the level or about 100yards ( 90
meters).
4. Too breathless to leave the house or breathless when dressing or undressing.

42. NYHA( NEW YORK HEART ASSOCIATION) CLASSIFICATION.
Class1.
● Ordinary physical activity doesn't cause undue fatigue, palpitation , dyspnea and / or
angina.
Class II .
● Ordinary physical activity does cause undue fatigue, palpitation , dyspnea and / or angina.
Class III
● Less than ordinary physical activity causes undue fatigue.
Class IV.
● Fatigue, palpitations , dyspnea and /or angina occur at rest.

43. PRECIPITATING AND RELIEVING FACTORS.
Precipitating factors.
● Exercise
● Exposure
● Occupational exposure
● Obesity
● Severe weight
● Medication .

44. RELIEVING FACTORS.
● Rest
● Medication.
Associated symptoms.
● Chest pain ( central, pleuritic or pericardial)
● Wheeze
● Fever
● Cough ( sputum production and colour)
● Change in pitch of voice
● Heart burn
● Hemoptysis.
● Muscle weakness or myalgia.
● Palpitation , syncope etc.

45. PHYSICAL EXAMINATIONS ( WHAT TO LOOK FOR).
General inspection.
● Anxiety may indicate anxiety disorder.
● Respiratory distress
● Ability to speak. Complete a sentence, unable to speak.
● Is there any audible wheeze or stridor ?. Is the voice Hoarse.
● Patient position
● Cyanosis or pallor.
● Mental status, it may be altered in hypoxemic and hypercapnic situations.

46. …
Vital signs.
Pulse : usually tachycardia , only bradycardia is in severe hypoxemia.
Respiratory rate .tachypnea danger if > 35 -40 beats per minute or below 10-12 beats per
minute.
Temperature . Is there fever.
Blood pressure, may increase if dyspnea is significant . Decrease may indicate life threatening
problem .
Pulseoximetry for any evidence of dessaturation

47. WHAT ELSE TO LOOK FOR IN GENERAL EXAMINATION.
 Finger clubbing (CA bronchus, Pulmonary fibrosis, Bronchietasis, Lung Abscess, Pleural
empyema, CHF, IE)
 Peripheral cyanosis- ( Cyanosis and clubbing may Indicate chronic severe hypoxia)
 Nasal polyps, septal deviation. Dyspnea due to nasal obstruction.
 Post nasal discharge- asthma/ allergy
 Jugular vein distension. Congestive heart failure , pulmonary oedema.
 Lower limb oedema . Cardiac problems

48. CHEST EXAMINATIONS.
● Normal chest is elliptical, increased in anterioposterior chest diameter ( may I dictate,
emphysema or COPD.
● Contraction of accessory muscles of respiration suggest severe difficulty in breathing.
● Retraction of supra clavicular fossa implies , tracheal stenosis.
● Pursed lip breathing and a prolonged expiratory phase are signs of outflow obstruction.
● Retraction of intercostal muscles on inspiration is characteristic of emphysema.
● Percuss for dullness or hyper resonance.

49. …
● Auscultate for wheeze (asthma, pulmonary oedema), quality of breath sounds.
● Crackles suggest fluid in the airway as it occurs with bronchitis, pneumonitis and CHF.
● Rhonchi, diminished breath sounds , rales.
NOTE. Normal chest examination findings does not rule out pulmonary pathology but only
lessen the likelihood that it is severe.

50. CARDIOVASCULAR EXAMINATION
Focus on :
● Signs of left sided heart failure
● Precordial impulse
● Detection of murmurs.( LHF , valvular dysfunction, S3- congestive HF.
● Signs of pulmonary hypertension and its consequences.
● Extremities for oedema and cyanosis.
Per abdomen.
Rule of ascites
Hepatojugular reflex.

51. INVESTIGATIONS.
1. Complete blood count. Assess for anemia and white cell counts.
2. Blood culture and sensitivity- identify probable pathogens
3. Sputum - Zn stain or Gene expert to rule out TB.
4. Arterial blood gas analysis- To assess the acid base status of the patient.
5. Electrolytes, BUN, creatinine, blood glucose. ( to ass6 metabolic derangement.

52. OTHER RELEVANT SPECIAL INVESTIGATIONS.
Chest xray.
● These has a great potential in aiding the diagnosis of many lung disorders that could have caused the
disorder and chest pain. ( consolidation, infiltrates masses ,cardiac size, hyperinflation, pneumonia, ILD
pleural effusion) etc.
Electocardiography
The ECG might be abnormal incase of structural heart disease. ( to assess left ventricular function and
pulmonary artery pressure) and if necessary a cardiopulmonary exercise test.
● Spirometry (lung volumes
● D.Dimers to rule of pulmonary embolism
● Ultra sound scan. To rule out acute cardiogenic pulmonary oedema.
If you suspect respiratory pump or gas exchange abnormalities , do a pulmonary function test . If diffusion
capacity reduced , consider CT angiogram.

53. MANAGEMENT OF A PATIENT WITH DYSPNEA.
Management strategy.
1. Reduce ventilatory demand
2. Decrease sense of effort
3. Improve respiratory muscle function
4. Pulmonary rehabilitation.

54. TREATMENT OF UNSTABLE PATIENT.
● Administer oxygen
● Consider intubation of the patient if gasping, apniec , or non unresponsive.
● Tension pneumothorax- thoracentesis
● Obstructive pulmonary disease - Bronchodilators
● Pulmonary oedema- IV / IM frusemide.
If the patient has stabilised.
● Reassess the patients airway, mental status , ability to speak and breathing effort.
● Check vital signs.
● Redo , thorough history taking , physical examination.

55. AFTER THE PATIENT HAS BEEN STABILISED
1. Reassess the patients airway, mental status, ability to speak and breathing efforts.
2. Check vital signs
3. Thorough history taking and physical examinations ( I.e breath sounds and observe skin
colour.

56. HOW DO WE REDUCE VENTILATORY DEMANDS .
Treat the underlying causes
● Infections
● Pleural effusion
● Pneumothorax
● Pulmonary embolism
● Congestive heart failure

57. HOMEWORK FROM LECTURE {CTRL OF RESPIRATION}
.

58. REFERENCES
● Davidsons Principles and practice of Medicine
● Oxford Handbook of Medicine
● Medscape