Pathophysiology Respiration

PATHOPHYSIOLOGY
RESPIRATORY SYSTEM
PATHOPHYSIOLOGY RESPIRATORY
RESPIRATORY SYSTEM - HOW WE BREATHE
▸ central chemoreceptors
https://www.khanacademy.org/science/health-and-medicine/respiratory-system/breathing-control-ir/v/
central-chemoreceptors
RESPIRATORY SYSTEM
▸ The ALVEOLI are the very small air sacs
that are the destination of air that you
breathe in.
▸ The CAPILLARIES are blood vessels

that are imbedded in the walls of the
alveoli. Blood passes through the
capillaries, brought to them by
the PULMONARY ARTERY
(Deoxygenated blood - CO2 rich) and
taken away by the PULMONARY
VEIN(Oxygenated blood - O2 rich).
▸ While in the capillaries, the blood

moves carbon dioxide into the alveoli
and takes up oxygen from the air in the
alveoli.
RESPIRATORY DISEASES
1. Acute respiratory disease: Influenza/colds, sinusitis
2. Obstructive pulmonary diseases: Asthma and COPD
3. Infections: Pneumonia and TB
4. Alterations in Pulmonary Vasculature
5. Cancer
WHO NCD
COUNTRY
PROFILE
2018
ZIMBABWE STATS
FLU AND COLDS

Acute
Respiratory
Illnesses
INFLUENZA
HOW INFLUENZA ENTERS THE BODY

FLU TRANSMISSION
▸ Through air droplets into the respiratory tract
▸ It may take one to four days after exposure to the influenza virus for symptoms to develop.
▸ An individual is contagious one day before developing symptoms and up to five to seven

days after becoming ill. Younger children or people with a weakened immune system may be
contagious for longer.
▸ Preventing tranmission;
1. staying home when sick
2. covering coughs and sneezes
3. washing hands often
4. routinely cleaning frequently touched surfaces
5. vaccination
Fig 1 Symptoms and complications of influenza.
Sam Ghebrehewet et al. BMJ 2016;355:bmj.i6258
©2016 by British Medical Journal Publishing Group

PATHOPHYSIOLOGY RESPIRATION
TREATMENT AND PREVENTION

▸ Vaccination:
▸ there are many different flu virus: vaccines protect against 3 to 4 viruses researched to be the most
common with an additional B virus component
▸ Influenza is usually self limiting in healthy individuals.
▸ Treatment of uncomplicated disease in healthy individuals is supportive and includes:

1. antipyretics eg paracetamol, ibuprofen
2. adequate fluid intake
3. rest -staying off work or school until 24 hours after resolution of fever to limit spread to others
4. lozenges
5. *decongestants
6. *antivirals
* special population grps

DIAGNOSIS/LABS
▸ clinical diagnosis at times when the virus is known to be circulating
▸ admitted patients may have respiratory samples taken for testing by :
1. PCR (polymerase chain reaction)-(is a rapid and sensitive method for

detecting the genetic material of influenza viruses, and is now the first-choice
laboratory test for influenza infection in both humans and animals.
2. Rapid antigen test - testing of respiratory secretions is widely used to confirm

the diagnosis of influenza with high sensitivity and specificity
3. Immunofluorescence assay - a staining of virus-infected cells in isolates is a

rapid and sensitive method to diagnose respiratory and other virus infections
4. Nasal swabs can be taken at start of outbreak to identify responsible organism

ANTIVIRAL TREATMENT
▸ For at risk individuals:
▸ Adults > 65yrs
▸ individuals with underlying chronic health conditions eg;CHF, lung, liver,

kidney, neurological and metabolic diseases such as Diabetes
▸ reduced immunity eg Cancer and HIV patients, asplenia, splenic dysfunction

prolonged steroid treatment
▸ Pregnant women, including up to 2 week post part
▸ morbidly obese individuals BMI >40
▸ as evaluated by clinician
Ref: NICE guidelines for hospitalised patients
COLD
‣ Flu and the common cold are both respiratory illnesses but they are
caused by different viruses.
‣ More than 200 types of viruses lead to colds, but the most common one is
the rhinovirus, which is thought to be responsible for at least 50% of colds.
Other viruses that can cause colds include coronavirus, respiratory
syncytial virus (RSV), influenza and parainfluenza
‣ Colds are usually milder than flu.
‣ People with colds are more likely to have a runny or stuffy nose.
‣ Colds generally do not result in serious health problems, such as
pneumonia, bacterial infections, or hospitalizations
‣ Being in cold weather does not cause the common cold but weather
promotes close contact
FLU VS COLD
CASE STUDY
▸ Max is a 37yr old pharmacist with a BMI = 45, who

presents with high fever(39C), sever muscle ache and
burning in the chest. He feels very unwell and cold.
▸
SINUSITIS
SINUSITIS
▸ acute sinusitis is typically preceded by a viral respiratory tract
infection that causes mucosal inflammation
▸ can be caused by bacteria -has similar s&s of viral
▸ obstructing sinus ostia-pathways that drain the sinus
▸ mucosal secretions are trapped, local defences are impaired and

bacteria from adjacent surfaces begin proliferation
▸ chronic sinusitis is caused by more persistent pathogens, it can

also precede an acute infection or there can be a subtle defect in
the hosts immune function
CLINICAL PRESENTATION
▸ non-specific upper respiratory tract infection that persists >7-14 days
Acute sinusitis :-
▸ nasal discharge/congestion
▸ maxillary tooth pain , facial/sinus pain that may radiate
▸ >7days is normally bacterial and should be treated with antimicrobials
▸ in children-nasal discharge and cough for >10-14 days or fever >39degrees or facial swelling and
pain are indication for antimicrobial therapy
Chronic sinusitis
‣ similar symptoms to acute but more specific
‣ rhinorrhea is assoc with acute exacerbations
‣ chronic unproductive cough and laryngitis w/wout headache
‣ infections occur 3-4 times a year and are unresponsive to steam and decongestants
TREATMENT
▸ Acute pts normally have spontaneous recovery
▸ antimicrobial therapy
*consider pt penicillin resistance
Non-Pharmcologic
‣ nasal decongestant sprays
‣ saline and steam
‣ mucolytics eg guaifenesin
‣ antihistamines
‣ internasal glucocorticoids
ASTHMA
ASTHMA
‣ affects airflow from bronchiole tubes to microscopic alveoli
‣ more common in developed countries with 5mil affected in the uk and with 1mil being children
‣ Intrinsic - normally adult onset with cryptogenic (hidden) effect
‣ Extrinsic - External causes normally as a result of allergens
‣ Allergies
‣ Atopic (Childhood onset)
‣ Asprin sensitive asthma - Aspirin inhibits Cox enzyme and shunting of arachidonic acid metabolism
through lipoxygenase pathway resulting in bronchoconstrictor leukotriene production
‣ Exercise induced asthma - hyperventilation = water +heat loss from pericellular lining fluid of
respiratory mucosa= triggers mediator release
‣ In adults later in life could be occupational; dangerous chemicals, pets, dust mites, cockroaches,
mold
‣ can also be related to gut bacteria (esp in children)

ASTHMA PATHOPHYSIOLOGY
AIRWAY HYPERACTIVITY
ACUTE SEVER ASTHMA

▸ ie: ‘Status Asthmaticus’
▸ non responsive to patient self treatment
▸ Resp rate: >25 breaths/min
▸ Tachycardia: > 100 beats/min
▸ peak expiratory flow rate 33-50% of their normal value
▸ Arterial Blood Gases are indicated when FEV1< 30%
▸ The four stages of SA are based on Arterial blood gases ABG
▸ Partial pressure of oxygen Pa02< 75mmHg
▸ Partial pressure of carbon dioxide PaC02> 38mmHg (> sign of resp muscle insufficiency)
▸ Arterial blood pH < normal (7.38 - 7.42) (Low pH-respiratory acidosis)
▸ Pulse Oximetry - measures oxygen saturation
▸ CBC - to rule out infectious disease, raised WBC - Eosinophils
▸ Serum electrolyte levels ; esp hypokalaemia (Side effect of drug therapy), low pH can cause transient elevation
▸ Serum glucose levels
▸ IgE levels in selected patients
▸ Electrocardiogram in older patients
▸ Blood theophylline if indicated

ASTHMA TREATMENT
▸ Corticosteroids
▸ Anticholinergics
▸ Short acting B2 agonists
▸ Oxygen - ventilator
Long term therapy
▸ Leukotriene modifiers
▸ Cromolyn
▸ Methylanthines
▸ Immunomodulators
▸ Coricosteroids
* immunotherapy eg allergy shots

ASTHMA CASE
▸ A 32yr old woman, Charity, arrives at the A&E with shortness of breath, complaining of tightness
in the chest and wheezing. Her respiratory rate is at 35breaths/min; Heart rate is 120beats/min.
She is unable to complete a sentence in 1 breath and not responding to her medication,
presents an albuterol inhaler. Her husband is holding their Labrador puppy as they were coming
from the SPCA. She was given therapy while her labs were taken
▸ Lab Results:
▸ PaO2 = 70mmHg
▸ PaCO2 = 55mmHg
▸ pH =7.22
▸ HCO3 = 25
Tmt plan;Hospital admission, treat asthma and respiratory acidosis, X dog

ABG QUICK TABLE
▸ Asthma ABGs
ASTHMA IN PREGNANCY
COPD
‣“Chronic" means long term, "obstructive" means it is hard to get air in and out of the lungs.
‣A patient with COPD may have either emphysema or chronic bronchitis, but many have
both. Some people with COPD may also have asthma.
‣A person who doesn't have enough alpha-1 antitrypsin, a major protein in the blood,
might have Alpha-1 Antitrypsin Deficiency, sometimes called Alpha-1. When Alpha-1
affects the lungs, it can cause COPD and is called inherited emphysema. And when it
affects the liver, it is called inherited liver disease.
COPD Causes:
‣85% of cases are caused by smoking cigarettes or being exposed to second hand smoke
or wood smoke in for long periods of time incl. during childhood
‣significant exposure to various types of dust such as coal, grain or wood or recurrent/
significant lung infections in infancy and early childhood  
COPD SYMPTOMS
▸ Increased severity of SOB
▸ cough/wheezing
▸ general feeling of ill health
▸ trouble sleeping (using more pillows or sleeping in a chair instead of a bed to avoid SOB)
▸ Increased sputum produced
▸ change in sputum color to yellow or green or presence of blood in sputum
▸ Increased fatigue and lack of energy that is persistent
▸ forgetfulness, confusion, slurring of speech and sleepiness

CHRONIC BRONCHITIS VS EMPHYSEMA
Chronic Bronchitis Emphysema
Mucus producing cough
Symptoms SOB
SOB
Chest tightness
Bronchodilators
Bronchodilators Steroids
Steroids Oxygen
Treatment Oxygen 
Antibiotics - in infection
Antibiotic-in infection
Pulmonary rehab
Pulmonary rehab Lung volume reduction surgery
Lung transplant
COMPENSATORY MECHANISM IN COPD

▸ Acute or chronic hypoxia in COPD
▸ Maintenance of ventilation-perfusion ratio by compensatory vasoconstriction
▸ an acute change occurring secondary to hypoxia is hypoxic pulmonary vasoconstriction
▸ Alveolar dead space in COPD results in inefficient gas exchange leading to ventilation
perfusion mis match
▸ the body tries to maintain V/Q ratio by localised vasoconstriction in the affected lung ares
without enough oxygen
▸ with the progression of COPD its cannot maintain a normal respiratory exchange as there is
reduced ability to exhale carbon dioxide leading to hypercapnia
▸ Chronic elevation CO2 over time leads to acid-base disorders and shift of normal respiratory
drive to hypoxic drive
COMPENSATORY MECHANISM IN COPD CONT..

▸ Hypercapnia and shift of normal respiratory drive to hypoxic drive to maintain respiratory
haemostasis.
▸ CO2 is normally the main stimulus for respiratory drive in normal physiologic states,
an increase in CO2 increases H+ ions which lower the pH
▸ chemoreceptors are more sensitive to alteration in acid - base balance
▸ increased arterial CO2 indirectly stimulates central chemoreceptors (medulla

oblongata) and directly stimulate peripheral chemoreceptors (carotid bodies and
aortic arch)
▸ chemoreceptors are less responsive to oxygen level in general, but in COPD its this is
blunted as the chemoreceptors develop tolerance to chronically elevated arterial CO2
levels - causing a shift in normal respiratory drive to hypoxic drive and low O2 levels
play the pivotal role in the stimulation of respiration through the chemoreceptors
and maintain respiratory hemostasis hence target PO = 88% to 92%

▸ Renal compensation
▸ to maintain a normal pH by retaining bicarbonate to neutralise pH
▸ the kidneys and the lungs are the key organs responsible for maintaining body pH
▸ The pH and the H+ concentration are determined by the ratio of HCO3/pCO2 and not by any single
value. This can be explained by Hasselbach equation pH = pK + log ([A ]/[HA])
a
-
▸ pH = 6.1 + log − HCO3/0.03pCO2
▸ The metabolic disorders and respiratory disorders lead to alteration in bicarbonate and pCO2
respectively. The body tries to maintain and minimize changes in the pH by kicking in the compensatory
mechanisms to keep the HCO3/pCO2 ratio constant. The compensation can be predicted to some extent
and is based on primary metabolic or respiratory disorder.
▸ In COPD patients, chronically elevated carbon dioxide shifts the normal acid-base balance toward acidic.
▸ There is retention of carbon dioxide which is hydrated to form carbonic acid. Carbonic acid is a weak and
volatile acid which quickly dissociates to form hydrogen and bicarbonate ions. This results in respiratory
acidosis.
▸ This primary event is characterized by increased pCO2 and fall in pH on arterial blood gas analysis.

▸ The response to acute and chronic respiratory acidosis is not to the same extent as both phases have a different
compensatory mechanism.
▸ In acute hypercapnia, only 1 mEq of HCO3 increases with every 10 mm Hg increase in pCO2. H+ ions buffering in
acute phase takes place by proteins (primarily hemoglobin) and other buffers (non-bicarbonate).
▸ H2CO3+ −Hb => HHb + −HCO3 
▸ The body has a mechanism to adapt to the adversities. The adjustment of the pH by the kidneys is much more
effective in chronic respiratory acidosis, and it can be better tolerated as compared to acute phase. In COPD
patients with comorbidities, mixed acid-base disorders can be seen.
▸ In chronic respiratory acidosis in COPD patients, the body tries to compensate by retaining more bicarbonate to
overcome acidosis. The renal compensation sets in and the kidneys adapt to excrete carbon dioxide in the form
of carbonic acid and reabsorb more bicarbonate. It usually takes about 3 to 5 days for the maximum response.
This helps in maintaining acid-base balance near normal and prevents the pH to become dangerously low.
▸ However, this effect is only at the blood level and not the brain. So, in long-term illness causing respiratory
acidosis,central nervous system (CNS) symptoms such as headache, anxiety, sleep disturbance, and drowsiness can
be seen.
▸
COMPENSATORY MECHANISMS
COPD DIAGNOSIS
• Spirometry: A spirometry test measures airflow in and out of the lungs. This indicates whether or not
there is airway obstruction.
• PFTs: find out more about the kind of COPD presented.
• Pulse oximetry: oxygen level in your finger.
◦ Exercise tolerance testing: The exercise tolerance test evaluates O2 needs and the level of activity
pt can perform
◦ Exercise for desaturation testing: The exercise for desaturation test evaluates if you may benefit
from supplemental oxygen at rest and during exercise.
• ABGs
• Bronchial provocation test: evaluates airway sensitivity. spirometry is done before and after inhale a
spray eg methacholine, results are compare pre and post spray to note changes in breathing.
• X-Rays and CT (CAT) Scans
• EKG and ECG, cardiac stress test
• mucus culture
• bronchoscopy
*Lung cancer screening
COPD MANAGEMENT
▸ Avoiding infections
▸ Medications: COPD bronchodilators, combination

bronchodilators and anti-inflammatories(steroids),
antibiotics
▸ Oxygen therapy
▸ Pulmonary Rehab
▸ Lung volume reduction surgery- sever emphysema

TYPES OF PFTS AND LUNG VOLUMES

• Spirometry/ Peak flow
• Lung volumes
• Diffusing capacity of monoxide
• Arterial blood gases

• Oximetry (oxygen saturation)
• 6 minute walk test
Picture from: pintrest.com

SPIROMETRY CONT…
-Tidal volume:(symbol VT or TV) is the lung volumerepresenting the normal volume of air displaced between normal inhalation and
exhalation when extra effort is not applied. In a healthy, young human adult,tidal volume is approximately 500 mL per inspiration or 7
mL/kg of body mass.
-Inspiratory reserve volume: the maximal amount of additional air that can be drawn into the lungs by determined effort after normal
inspiration
-Expiratory reserve volume: the additional amount of air that can be expired from the lungs by determined effort after normal
expiration
-RV:…
-TLC:…
-FRC:…
FORCED EXPIRATORY VOLUME (FEV)

• Most commonly used measure to assess lung function (obstruction)
• Measure vital capacity
• Person breathes in as deeply as possible, the breathes out with as much
force as possible
• Use the best of 3 tries
• Compare with normal values or assess patients progress against their last
reading.
Classification of Obstruction Level of impairment
Mild 75% of normal function

Moderate <60% of normal function
Severe <40%
SPIROMETRY CONT…
MODEL OF ANNUAL DECLINE OF FEV1 REC

EMPHYSEMA
COPD’s pathology includes loss of tissue elasticity, emphysematous bullae, small airway obstruction, and destruction
of lung parenchyma. Persons with COPD are typically separated into one of two catagories: “pink puffers” (normal
PaCO2, PaO2 > 60 mmHg) or “blue bloaters” (PaCO2 > 45 mmHg, PaO2 < 60 mmHg). Pink puffers have severe
emphysema, and characteristically are thin and free of signs of right heart failure. Blue bloaters, on the other hand,
have frequent episodes of right heart failure, and produce copious sputum resulting in coughing and respiratory
infections. Blue bloaters presents more of a chronic bronchitis picture although they too may exhibit emphysematous
changes.
Pink puffers (normal PaCO , PaO > 60 mmHg) have emphysematous lung tissue destruction. Diffusing capacity is
2 2
decreased by destroyed pulmonary capillaries. ABG’s are near normal due to compensatory hyperventilation. The
only subtle changes typically are a PaO slightly depressed (often in the mid 70’s, resulting in mild pulmonary
2
vasoconstriction), and a low-normal PaCO . 2
Blue bloaters (PaCO > 45 mmHg, PaO < 60 mmHg) suffer from pulmonary hypoxic vasoconstriction from the
2 2
marked hypoxia and respiratory acidosis. This in turn leads to right ventricular hypertrophy and cor pulmonale. The
right heart failure then leads to systemic venous congestion, peripheral edema, hepatic congestion, and ascites.
Secondary erythrocytosis may occur, spurred by the hypoxia. Changes on ABG’s are much more pronounced.
EMPHYSEMA
Jim B., a 68-year-old man here for his Phase II Pulmonary Rehabilitation intake interview.
TEXT
Medical history: COPD, FEV1 six weeks ago was 38% of normal predicted, recent CXR shows flattened diaphragm with increased AP diameter,
appendectomy age 34, broken nose and broken right arm as a child.
Labs: Lytes plus and CBC all within normal limits
Physical exam: Breath sounds markedly diminished bilaterally with crackles right lower lobe and wheeze left upper lobe. Visible use of
accessory muscles. O2 Saturation 93% room air, 95% O2 on 2lpm. Respiratory rate 24 and shallow, HR 94, BP 150/88, 1+ pitting pedal edema.
Current Medications: Prednisone 10mg q day / DuoNeb q 4 hrs. / Ibuprofen 400mg BID / Tums prn (estimates he takes two per day).
Respiratory history: 80-pack-year cigarette history, quit last year. He has developed a dry, hacking, non-productive cough over the last six
months. Had asthma as a child and was exposed to second-hand smoke and cooking fumes while working at family-owned restaurant as a child.
Lately, he has noticed slight chest tightness and increased cough when visiting his wife’s art studio.
Family history: Father had emphysema, died at age 69, mother died of breast cancer at 62. Grandfather died at age 57, grandmother died in
her 40s of suicide. Six adult children, alive and well.
Previous respiratory admissions: Inpatient admission for six days last winter for acute exacerbation of COPD with bacterial pneumonia
requiring 24-hour intubation and mechanical ventilation.
Psych: Jim presents to his Phase II Pulmonary Rehab intake interview appearing disheveled, wearing a sweatshirt, pajama pants and bedroom
slippers. He is accompanied by his wife and adult daughter who appear neat, clean and well dressed. Patient states, “I don’t think you people
can do anything to help me. I’m only here because they (referring to wife and daughter) made me go.” Jim states that he has been doing less
and less at home since discharged from the hospital last winter. Wife states, “He walked outside a little with our grandchildren last Sunday and
got so short of breath, he almost collapsed.” Became emotional when saying, “It scared the kids. It tore me up for them to see me that way.
Besides that, with this darn shoulder I can’t even pick up the little ones anymore.”
Social: Lives at home with his wife of 43 years who works as an artist. Two out of his six children live within 30 miles of Jim’s home.
Occupation: Building contractor, retired three years ago. Jim states, “I made a good living. All the kids were able to go to college. I was strong. I
could work circles around anybody in my crew. And now look at me. I’m tied to that darn breathing machine (referring to nebulizer) and I might
as well hang it up.” Wife states, “He used to have all kinds of energy. Now all he does is sit in his chair watching TV, eating potato chips and
peanuts.”
PNEUMONIA
Pneumonia is an infection that inflames the air sacs
in one or both lungs.
The air sacs may fill with fluid or pus (purulent

material), causing cough with phlegm or pus, fever,
chills, and difficulty breathing.
A variety of organisms, including bacteria, viruses

and fungi, can cause pneumonia.
Pneumonia can range in seriousness from mild to

life-threatening. It is most serious for infants and
young children, people older than age 65, and
people with health problems or weakened
immune systems.
The signs and symptoms of pneumonia vary from

mild to severe, depending on factors such as the
type of germ causing the infection, and your age
and overall health. Mild signs and symptoms often A classic sign of bacterial pneumonia is a cough that produces thick,
are similar to those of a cold or flu, but they last blood-tinged or yellowish-greenish sputum with pus.
longer.
LOBULAR PNEUMONIA STAGES
▸ Congestion -
▸ Red Hepatization -
▸ Grey Hepatization
▸ Resolution -
COMPENSATORY MECHANISMS
▸ vasoconstriction of Pulmonary arterioles
▸ Tachypnea - rapid breathing (due to hypoxemia)
▸ Refractory hypotension
▸ ref: V/Q ventilation perfusion ratio
▸ hypercapnia
PNEUMONIA SIGNS AND SYMPTOMS

May include:
• Abrupt onset of Fever, sweating and shaking chills

• Rust coloured sputum or Hemopysis
• Pleuritic chest pain
• Chest pain when you breathe or cough
• Confusion or changes in mental awareness (in adults age 65 and older)
• Cough, which may produce phlegm
• Fatigue
• Lower than normal body temperature (in adults older than age 65 and people with weak immune
systems)
• Nausea, vomiting or diarrhea
• Shortness of breath
• Newborns and infants may not show any sign of the infection. Or they may vomit, have a fever and
cough, appear restless or tired and without energy, or have difficulty breathing and eating.
PNEUMONIA SIGNS AND SYMPTOMS CONT..

▸ Physical examination
▸ tachypnea and tachycardia
▸ dullness to percussion
▸ increased tactile fremitus (assessment of the lungs by either the

vibration intensity felt on the chest wall )
▸ Chest wall retractions and grunting respirations
▸ diminished breath sounds over affected area
▸ inspiratory crackles during lung expansion

DIAGNOSIS
▸ Chest X-ray - extent and location
▸ dense lobar or segmental infiltrate
▸ Blood test - confirmation and ID
▸ leukocytosis with predominance of polymorphonuclear cells, serum K, PaCO2, PaO2
▸ Pulse oximetry
▸ low O2 sat
▸ Sputum test - to pinpoint cause of infection for antibiotic/virus/fungal
▸ CT scan - more detailed image of lung if clearing is not as quick
▸ Pleural fluid culture - taken by putting a needle between your ribs from pleural area, also analysed
to determine infection type
▸
TYPES OF PNEUMONIA
1. Community acquired Pneumonia
2. Hospital/Nosocomal Pneumonia
3. Healthcare associated pneumonia (HCAP)
4. Aspiration acquired
COMMUNITY ACQUIRED PNEUMONIA (CAP)

▸ most common pneumonia type
Causes:
▸ Bacteria eg S.Pneumoniae
▸ Mycoplasma - M.Pneumoniae (walking pneumonia)
▸ Fungi - esp in chronic health problems or weakened immune systems (found in soil or bird droppings)
▸ Virus - eg;influenza, most common in children <5yrs

Treatment
▸ Outpatients : Macrolide/azalide, doxycycline or fluoroquinolone
▸ Inpatient/general medical ward : Extended-spectrum cephalosporin + macrolide/azide or
B-Lactam/B-Lactamse inhibitor + macrolide/azalide or fluoroquinolone
▸ Inpatient/intensive care unit : Extended spectrum cephalosporin or B-lactam/B-lactamse inhibitor +

fluoroquinolone or Macrolide/azalide
HOSPITAL(NOSOCOMIAL) ACQUIRED PNEUMONIA

▸ bacterial infection acquired during hospital stay for another illness
▸ greater propensity for drug resistance
▸ patients on ventilators eg; intensive care units are at high risk

Treatment:
1. * RESISTANCE
▸ B-Lactams - some were developed for multiple antibiotic resistant hospital organisms but they
themselves induce broad spectrum B-lactamase and thereby lead to greater problems with
resistance eg: MRSA
▸ hence site specific preference
▸ there are newer drugs but expensive

2. Diet
‣ Many patients with nosocomial pneumonia have significant nutritional deficiencies. Early (within
48 hours) enteral nutrition appears to decrease infectious complications. Parenteral nutrition
does not seem to have this effect and should be considered only in patients with a
contraindication to enteral replacement
HEALTHCARE ACQUIRED PNEUMONIA

▸ defined as pneumonia in nonhospitalized patients who had significant experience with the healthcare system.
▸ Such contact could include
1. Intravenous therapy for wound care within the preceding 30 days,
2. Residence in a long-term care facility,
3. Hospitalization in an acute-care hospital within the preceding 90 days, and/or
4. Outpatient treatment in a hospital or hemodialysis clinic within the preceding 30 days.
▸ These individuals were believed to be at an increased risk for infection with multidrug-resistant (MDR)
organisms because of such contact. However, more recent studies have indicated that many individuals who
[
met the criteria for HCAP were not infected with MDR pathogens. The risk of infection with MDR organisms
[2]
appears to depend much more on specific risk factors of the given patient than on contact with various aspects
of the healthcare system.
Treatment
▸ Patients who would have met the criteria for HCAP should not be empirically treated with antibiotics to cover
MDR bacteria unless they have valid risk factors for acquiring MDR organisms can be caused by bacteria more
resistant to antibiotics
ASPIRATION PNEUMONIA
▸ occurs when food, drink, vomit and saliva is inhaled into

lungs
▸ occurs when gag reflex is disturbed eg;brain injury,

excessive alcohol or drugs
Treatment
1. supportive care for breathing
2. Antibiotics
PNEUMONIA IN SPECIAL CLINICAL CIRCUMSTANCES

HIV
▸ HIV infects and destroys helper T-Lymphocytes bearing the CD4 surface
molecule wc is critical for a wide range of immunologic responses
▸ depletion results in dysfunction of both cell mediated and humoral

immunity thus a broad range of substances can cause multiple
occurrence of pneumonia in HIV pts
▸ Treatment : Antibiotics
▸
GENERAL PNEUMONIA TREATMENT

▸ after consideration of resp function, dehydration, general illness or sepsis
▸ O2 (humdified O2 for hypoxemia)
▸ bronchodilators - with bronchospasm
▸ chest physiotherapy
▸ rehydration
▸ Antipyretics/anti-inflammatories
▸ Antibiotics
Refer to NICE Guidlines

CHIEF COMPLAINT: Cough and fever for four days
HISTORY: Mr. Alcot is a 68 year old man who developed a harsh, productive cough four days prior to being seen by a physician. The
sputum is thick and yellow with streaks of blood. He developed a fever, shaking, chills and malaise along with the cough. One day
ago he developed pain in his right chest that intensifies with inspiration. The patient lost 15 lbs. over the past few months but claims
he did not lose his appetite. "I just thought I had the flu." Past history reveals that he had a chronic smoker's cough for "10 or 15
years" which he describes as being mild, non-productive and occurring most often in the early morning. He smoked 2 packs of
cigarettes per day for the past 50 years. The patient is a retired truck driver who has been treated for mild hypertension, bronchitis,
appendicitis (as a young adult), hemorrhoids and a fractured femur and splenic injury (motorcycle accident).
PHYSICAL EXAMINATION: The patient is an elderly man who appears tired haggard and underweight. His complexion is sallow.
He coughs continuously. Sitting in a chair, he leans to his right side, holding his right chest with his left arm. Vital signs are as follows:
blood pressure 152/90, apical heart rate 112/minute and regular, respiratory rate 24/minute and somewhat labored, temperature
102.6<sup>o</sup>F. Examination of the neck reveals a large, non-tender hard lymph node in the right supraclavicular fossa. Both
lungs are resonant by percussion with one exception: the right mid-anterior and right mid-lateral lung fields are dull. Auscultation
reveals bilateral diminished vesicular breath sounds. Bronchial breath sounds, rhonchi and late inspiratory crackles (are heard) in the
area of the right mid-anterior and right mid-lateral lung fields. The remainder of the lung fields is clear. Percussion and auscultation
of the heart reveals no significant abnormality. Examination of the fingers shows clubbing.
LABORATORY: WBC 17,000/mm3; neutrophils 70%, bands 15%, lymphocytes 15%.
COURSE OF ILLNESS: Following a chest x-ray PA view and Lateral which revealed an acute pneumonia in the right middle lobe, the
patient was treated with antibiotics as an outpatient. During the 10 days of treatment the patient's fever abated and he felt
somewhat better. A post-treatment (follow up) chest x-ray reveals a right hilar mass. Sputum cytology demonstrates atypical cells.
1.Review the lab findings. What is your diagnosis?
2. What do you understand by the terms "hospital acquired" and "community acquired " pneumonia.? Which type of
pneumonia does our patient have?
3. What organisms are likely to be causing his pneumonia?
4. List the various host factors, or conditions which predispose a patient to developing pneumonia. What host factors may
have predisposed this patient to pneumonia?
5. Is prevention possible?
TUBERCULOSIS
▸ most prevalent communicable disease
▸ Co-infection with HIV accelerates the progression of both diseases
▸ can produce atypical S&S in infants , elderly and immunocompromised hosts
▸ caused by mycobacteria, these are slow growing organisms and require special
stains, growth media, and long periods of incubation to isolate and identify
▸ M.Tuberculosis is the typical pathogen
▸ a latent TB infection can lead to reactivation disease years after the primary
infection occurred
▸ once pt is diagnosed or suspected they should be isolated in -ve pressure

hospital rooms
TUBERCULOSIS
Signs and symptoms
▸ weight loss
▸ fatigue
▸ productive cough
▸ hemoptysis
▸ fever and night sweats
Labs/diagnosis
‣ moderate elevations in WBC with lymphocyte predominance
‣ chest xray: patchy or nodular filtrates apical arena of upper lobes or the superior segment
of lower lobes (cavitation that may show air-fluid levels as the infection progresses
‣ skin testing
TREATMENT
▸ administer multiple drugs which the organism is susceptible to
▸ adding 2 new agents to drug regimen to which organism is

susceptible
▸ safest most effective therapy for the shortest period of time
▸ ensuring adherence to therapy by utilising directly observed

therapy (Non adherence to therapy due to ADR is major cause
of treatment failure)
▸ HIV(-) pts normally 6-9months of therapy

REACTIVATION
▸ occurs in 10% of pts within 2 years of infection
▸ refer to EDLIZ or MOH TB guidlines for treatment

TB IN HIV CASE STUDY

A 42 year-old male living with HIV was identified as a close contact to his girlfriend who was recently diagnosed with TB disease. He was contacted by the local health department
for TB screening. The nurse assessment revealed a medical history of HIV, hypertension, a peptic ulcer, and occassional alcohol consumption. His physical exam was unremarkable.
A symptom screen and a CXR were performed to rule out active TB disease and the results indicated no evidence of active TB.
1. Which TB screening test should he initially be evaluated with?

A.TST
B.IGRA
C.A and B
D.A or B
2. The local health department nurse decided to place a TST that resulted in a 6 mm induration. What action should be taken next?
A.Repeat the TST because it is not reliable in this population.
B.Confirm the TST with an IGRA test
C.Send patient for CXR
D.Nothing, because the TST result is negative and TB infection can be ruled out.
3. A symptom screen and a CXR were performed to rule out active TB disease and the results indicated no evidence of active TB. How should this patient be classified?
A.Class 0 - No TB exposure, not infected.
B.Class 1 - TB exposure, no evidence of infection.
C.Class 2 - TB infection, no TB disease.
D.Class 5 - TB suspected. The patient was diagnosed with TB infection.
4. Based on the patient’s HIV treatment, the health department decided to treat with rifabutin for four months. What should be done prior to initiating TB infection treatment?
A.Place the patient in respiratory isolation.
B.Baseline hearing screening.
C.Baseline visual acuity.
D.Obtain baseline laboratory testing for liver function tests (LFTs).
His baseline liver enzyme results came back, Due the patient’s elevated liver enzymes at baseline, what is the next step?
•AST (SGOT) - 104 units/L (normal 0-37 units/L)
•ALT (SGPT) - 127 units/L (normal 0-40 units/L)
•Total Bilirubin - 1.0 mg/dL (normal 0.3-1.0 mg/dL)
A.Encourage patient to abstain from alcohol use and recheck LFTs in one week.
B.Give patient prescription for 1 month supply of RFB.
C.Immediately refer the patient to an alcohol treatment program.
D.Give patient prescription for 1 month supply of INH.
REFLECTION
‣ In this scenario, the patient’s TST resulted in a 6 mm induration which is classified as positive
for those who are identified as contacts to a person diagnosed with a contagious form of
tuberculosis as well as a person with an immunocompromising condition such as HIV. However,
a negative TST (induration < 5 mm) does not exclude the diagnosis of TB (especially for
patients with severe TB illness or infection with HIV).
‣ Patients with HIV who may not react to testing by TST or IGRA should have a chest x-ray and
medical evaluation if TB is suspected or if exposed to active TB disease. If abnormalities are
noted, or the client has symptoms suggestive of extrapulmonary TB, additional diagnostic tests
should be conducted.
‣ In HIV-infected individuals, almost any abnormality on CXR may be indicative of TB.
‣ Completion rates with INH for 9 months are much lower than shorter regimens such as rifabutin
for four months which show higher completion rates. When using rifampin or rifabutin, it is
important to remember to check for potential drug-drug interactions. INH is a treatment option
in persons who have medication interactions that do not allow use of a rifamycin. Patients who
are taking INH with their other medications prescribed on a long-term basis or who use alcohol
regularly should be monitored closely.
PULMONARY HYPERTENSION
▸ pulmonary circulation is a high flow, low pressure system - 25/8mmHg
▸ PH is the sustained increase in arterial pressure >30mmHg systolic; in some cases 60-100mmHg
▸ 2 types:
1. Primary (Idiopathic) - PPH
2. Secondary
In PH tiny arteries in the lungs, called pulmonary arterioles, and capillaries become narrowed, blocked or
destroyed. This makes it harder for blood to flow through the lungs, and raises pressure within the lungs' arteries.
As the pressure builds, the heart's lower right chamber (right ventricle) must work harder to pump blood through
the lungs, eventually causing heart muscle to weaken and fail. Some forms of pulmonary hypertension are serious
conditions that become progressively worse and are sometimes fatal. Although some forms of pulmonary
hypertension aren't curable, treatment can help lessen symptoms and improve your quality of life.
PATHOPHYSIOLOGY
CAUSES OF PULMONARY HTN

PRIMARY (IDIOPATHIC) - PH
▸ cause is unknown ie idiopathic but can be associated with portal HTN
and cirrhosis, appetite suppressant drugs and HIV, could be familial
▸ poor long term prognosis difficult to treat
▸ more common in women than in men 1.7:1
▸ presents in 3rd to 4th decade of life
▸
SECONDARY PULMONARY HTN

▸ caused by known disease process or pathophysiologic
condition
As a result of 3 major mechanisms
1. increased pulmonary blood flow
2. increased resistance to blood flow
3. increased left arterial pressure

SIGNS AND SYMPTOMS OF PH

‣ Shortness of breath (dyspnea), initially while exercising and eventually while at rest
‣ Fatigue
‣ Dizziness or fainting spells (syncope)
‣ Chest pressure or pain
‣ Swelling (edema) in your ankles, legs and eventually in your abdomen (ascites)
‣ Bluish color to your lips and skin (cyanosis)
‣ Racing pulse or heart palpitations
‣
CLINICAL DIAGNOSIS
• Echocardiogram.
• Exercise stress tests may be done.
• Chest X-ray.
• Electrocardiogram (ECG).
• Right heart catheterization - a cardiologist places a thin, flexible tube (catheter) into a vein in neck or groin. The catheter is
then threaded into the right ventricle and pulmonary artery. This procedure directly measures the pressure in the main
pulmonary arteries and right ventricle. It's also used to see what effect different medications may have on pulmonary
hypertension.
• Blood tests.
• Additional tests to check the condition of lungs and pulmonary arteries and determine the cause of condition, includes:
• Computerized tomography (CT) scan - (CT angiography).
• Magnetic resonance imaging (MRI).
• Pulmonary function test - spirometer.
• Polysomnogram- detects brain activity, heart rate, blood pressure, oxygen levels and other factors while patient is asleep.
• Ventilation/perfusion (V/Q) scan.
• Open-lung biopsy - very rare; to analyse secondary cause of pulmonary hypertension.
• Genetic tests
PH CLASSIFICATION
Pulmonary hypertension classification
• Class I. No symptoms with normal activity.
• Class II. No symptoms at rest, but symptoms such as fatigue, shortness of breath or chest pain with normal activity.
• Class III. Comfortable at rest, but symptoms with physical activity.
• Class IV. Symptoms with physical activity and at rest.

TREATMENT
Palliative care
Pulmonary hypertension can't be cured, but doctors can help manage the condition.
Treatment may help improve symptoms and slow the progress of pulmonary hypertension.
It often takes some time to find the most appropriate treatment for pulmonary hypertension. The treatments are often complex
and require extensive follow-up care. The patient might need to change their treatment if it's no longer effective.
When pulmonary hypertension is caused by another condition, treat the underlying cause whenever possible.
PHARMACOTHERAPY
• Blood vessel dilators (vasodilators). Vasodilators open narrowed blood vessels.
epoprostenol (Flolan, Veletri) - effects last only a few minutes. This drug is continuously injected through an intravenous (IV) catheter via a small pump worn in a
pack on a belt or shoulder. Potential side effects of epoprostenol include jaw pain, nausea, diarrhea and leg cramps, as well as pain and infection at the IV site.
iloprost (Ventavis), can be inhaled six to nine times a day through a nebulizer, a machine that vaporizes medication. Because it's inhaled, it goes directly to the
lungs. Side effects associated with iloprost include chest pain — often accompanied by a headache and nausea — and breathlessness.
Treprostinil (Tyvaso, Remodulin, Orenitram), another form of the drug, can be given four times a day. It can be inhaled, taken as oral medication or administered
by injection. It can cause side effects such as a headache, nausea and diarrhea.
• Endothelin receptor antagonists. These medications reverse the effect of endothelin, a substance in the walls of blood vessels that causes them to narrow. These
drugs may improve energy level and symptoms. However, these drugs shouldn't be taken in pregnancy. Also, these drugs can damage the liver and pt may need
monthly liver monitoring.eg bosentan (Tracleer), macitentan (Opsumit), and ambrisentan (Letairis).
• Sildenafil (Revatio, Viagra) and tadalafil (Cialis, Adcirca) are sometimes used to treat pulmonary hypertension. These drugs work by opening the blood vessels in
the lungs to allow blood to flow through more easily. Side effects can include an upset stomach, headache and vision problems.
• High-dose calcium channel blockers. These drugs help relax the muscles in the walls of blood vessels. They include medications such as amlodipine (Norvasc),
diltiazem (Cardizem, Tiazac, others) and nifedipine (Procardia, others). Although calcium channel blockers can be effective, only a small number of people with
pulmonary hypertension respond to them.
• Soluble guanylate cyclase (SGC) stimulator. Soluble guanylate cyclase (SGC) stimulators (Adempas) interact with nitric oxide and help relax the pulmonary
arteries and lower the pressure within the arteries. These medications should not be taken in pregnancy. They can sometimes cause dizziness or nausea.
• Anticoagulants. warfarin (Coumadin, Jantoven) to helps prevent the formation of blood clots within the small pulmonary arteries. Because anticoagulants prevent
normal blood coagulation, they increase risk of bleeding complications. Warfarin must be taken exactly as prescribed, because warfarin can cause severe side
effects if taken incorrectly. Periodic blood tests to check how well the drug is working are done. Many other drugs, herbal supplements and foods can interact with
warfarin.
• Digoxin. Digoxin (Lanoxin) can help the heart beat stronger and pump more blood. It can help control the heart rate in pts with arrhythmias.
• Diuretics. Commonly known as water pills, these medications help eliminate excess fluid from your body. This reduces the amount of work the heart has to do. They
may also be used to limit fluid buildup in lungs.
• Oxygen. A treatment known as oxygen therapy, to help treat pulmonary hypertension, especially for pts living at a high altitude or with sleep apnea. Some people
who have pulmonary hypertension eventually require continuous oxygen therapy.
OTHER TREATMENT
Surgeries
Atrial septostomy.
• If medications don't control your pulmonary hypertension, this open-heart surgery might be an option. In an atrial
septostomy, a surgeon will create an opening between the upper left and right chambers of your heart (atria) to relieve the
pressure on the right side of your heart. 
Atrial septostomy can have serious complications, including heart rhythm abnormalities (arrhythmias). 
Transplantation.
• In some cases, a lung or heart-lung transplant might be an option, especially for younger people who have idiopathic
pulmonary arterial hypertension. 
Major risks of any type of transplantation include rejection of the transplanted organ and serious infection, and you must take
immunosuppressant drugs for life to help reduce the chance of rejection. 
PULMONARY EMBOLISM
▸ Caused by undissolved detached material that occludes blood vessels of the primary vasculature, as a result
circulation distal to the obstruction is impaired
▸ of those who experience fatal PE, 8-10% die within an hour of onset of symptoms
▸ more than 90% pulmonary thromboemboli originate in the deep veins of lower extremities
▸ Embolism types:
1. Thrombotic
2. Fat
3. Amniotic fluid
4. Air
5. Tumor
6. Foreign material
7. Septic
8. Parasitic
VIRCHOWS TRIAD
▸ factors that predispose patients to thrombus formation,

increasing risk of PE
1. Venous stasis/sluggish blood
2. Hypercoagulability
3. Damage to venous wall
The most common risk factors are immobility, trauma,

pregnancy, cancer, heart failure and estrogen use
THROMBOEMBOLISM
▸ https://www.youtube.com/watch?v=CfjGhwQiDOE
CLINICAL FEATURES AND DIAGNOSIS

▸ depends on size of emboli
▸ initially, restlessness, apprehension and anxiety with dyspnea, tachycardia and tachypnea
▸ medium sized to massive - sudden dyspnea and sever chest pain(plueritic(infarction) or non-pleuritic) pain worse
with deep breath
▸ pain on inspiration
▸ may or may not have hemoptysis
▸ as it worsens; heart failure, respiratory arrest and shock

Diagnosis
▸ V/Q lung scan within 8 hrs of onset
▸ ABG analysis
▸ ECG - abnormal in 85% of cause
▸ Chest radiographs
▸ Cardiac enzymes
▸ pulmonary arteriography * the only conclusive diagnostic test
▸ duplex ultrasound to determine site of DVT

TREATMENT
▸ primary treatment is prevention -compression socks,socks, range of motion exercises or
prophylaxis;
▸ low dose subQ sodium heparin or
▸ low-molecular-weight heparins eg fragmin, dalteparin
▸ in suspected or confirmed PE
▸ supplemental O2 with activity limitations
▸ loading dose Heparin maintaining appt(activated partial thromboplastin time) of 1.5-2.5
▸ thrombolytic therapy
▸ inferior vena cava filters
▸ embolectomy in life threatening emergency pt with refractory hypertension

NICE CASE STUDY 1

https://www.nice.org.uk/guidance/cg144/resources/pulmonary-embolism-clinical-case-scenarios-pdf-format-pdf-186678400
LUNG CANCER
LUNG CANCER
▸ Leading cause of cancer death in both male and female patients in the US
with a 5 year survival rate of 15%
▸ Cigarette smoking is responsible for 83%
▸ Non-small cell lung cancer (NSCLC) is diagnosed in the majority 80% of its
▸ NSCLC has a slower growth rate and doubling time than Small cell lung
cancer (SCLC)
▸ many go undetected until advanced due to unnoticeable early signs of

dyspnea and cough
▸ large tumors and metastatic disease prompt medical attention

CLINICAL PRESENTATION
▸ Signs and symptoms

1. primary tumor
2. regional spread
3. metastatic spread
4. pareneoplastic syndrome
5. associated histology
LUNG CANCER TREATMENT

▸ Depends on stage
▸ may include
▸ Surgery
▸ Chemotherapy
▸ Radiation therapy
▸ Targeted drug therapy
▸ Immunotherapy
MATERIAL WAS ADAPTED FROM

▸ NICE Guidelines
▸ GOLD guidelines
▸ BMJ
▸ WHO
▸ NCBI
▸ NIH
▸ Copstead.L.C and Banasik. J. L. Pathophysiology 3rd edition
▸ Goodman and Gillman’s. The Pharmacological Basis of Therapeutics
▸ Dipiro et al Pharmacotherapy a physiologic approach
▸ Koda Kimble
▸

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Pathophysiology Respiration

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PATHOPHYSIOLOGY

RESPIRATORY SYSTEM - HOW WE BREATHE

▸ The CAPILLARIES are blood vessels

▸ While in the capillaries, the blood

2. Obstructive pulmonary diseases: Asthma and COPD

3. Infections: Pneumonia and TB

4. Alterations in Pulmonary Vasculature

FLU AND COLDS

HOW INFLUENZA ENTERS THE BODY

▸ An individual is contagious one day before developing symptoms and up to five to seven

1. staying home when sick

2. covering coughs and sneezes

3. washing hands often

4. routinely cleaning frequently touched surfaces

Sam Ghebrehewet et al. BMJ 2016;355:bmj.i6258

©2016 by British Medical Journal Publishing Group

TREATMENT AND PREVENTION

▸ Influenza is usually self limiting in healthy individuals.

▸ Treatment of uncomplicated disease in healthy individuals is supportive and includes:

2. adequate fluid intake

* special population grps

▸ admitted patients may have respiratory samples taken for testing by :

1. PCR (polymerase chain reaction)-(is a rapid and sensitive method for

2. Rapid antigen test - testing of respiratory secretions is widely used to confirm

3. Immunofluorescence assay - a staining of virus-infected cells in isolates is a

4. Nasal swabs can be taken at start of outbreak to identify responsible organism

▸ Adults > 65yrs

▸ individuals with underlying chronic health conditions eg;CHF, lung, liver,

▸ reduced immunity eg Cancer and HIV patients, asplenia, splenic dysfunction

▸ Pregnant women, including up to 2 week post part

▸ morbidly obese individuals BMI >40

▸ Max is a 37yr old pharmacist with a BMI = 45, who

▸ can be caused by bacteria -has similar s&s of viral

▸ obstructing sinus ostia-pathways that drain the sinus

▸ mucosal secretions are trapped, local defences are impaired and

▸ chronic sinusitis is caused by more persistent pathogens, it can

▸ maxillary tooth pain , facial/sinus pain that may radiate

▸ >7days is normally bacterial and should be treated with antimicrobials

‣ rhinorrhea is assoc with acute exacerbations

‣ chronic unproductive cough and laryngitis w/wout headache

‣ nasal decongestant sprays

‣ saline and steam

‣ Intrinsic - normally adult onset with cryptogenic (hidden) effect

‣ Extrinsic - External causes normally as a result of allergens

‣ Atopic (Childhood onset)

‣ can also be related to gut bacteria (esp in children)

ACUTE SEVER ASTHMA

▸ non responsive to patient self treatment

▸ Resp rate: >25 breaths/min

▸ Tachycardia: > 100 beats/min

▸ peak expiratory flow rate 33-50% of their normal value

▸ Arterial Blood Gases are indicated when FEV1< 30%

▸ The four stages of SA are based on Arterial blood gases ABG

▸ Partial pressure of oxygen Pa02< 75mmHg

▸ Arterial blood pH < normal (7.38 - 7.42) (Low pH-respiratory acidosis)

▸ Pulse Oximetry - measures oxygen saturation

▸ CBC - to rule out infectious disease, raised WBC - Eosinophils

▸ Serum glucose levels

▸ IgE levels in selected patients

▸ Electrocardiogram in older patients

▸ Blood theophylline if indicated

▸ Short acting B2 agonists

* immunotherapy eg allergy shots

Tmt plan;Hospital admission, treat asthma and respiratory acidosis, X dog

▸ H2CO3+ −Hb => HHb + −HCO3 