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Chapter 6 Selected Diseases and Disorders of the Respiratory System

Chapter 6 Respiratory Diseases and Disorders – Sakshi

Zoë Soon

Creative Commons –  Simple Pictures, Images, Video Clips, and/or Gifs that help illustrate any of the following:

*For diseases we discuss:

a) Basic Risk Factors

b) Most Common signs and symptoms

c) Basic Pathology, with basic diagnostic tools (e.g. imaging, blood tests) and basic treatment

 

1 – Review of Respiratory System Anatomy

Different ways of breathing.
Figure 1 – Represents three different respiratory systems, all performing the same role, i.e., exchange of gases.

 

Represents the major respiratory organs in the human body
Figure 2 – Represents the major respiratory organs in the human body.

 

Figure 3 – Represents the upper respiratory tract (upper airway)

 

Figure 4 – Gross anatomy of the human lungs, showing the right and left lobes.

 

Figure 5- Represents main parts of the respiratory zone i.e., alveolus is responsible for gas exchange.

 

Figure 6 – Pseudostratified Ciliated Columnar Epithelium. Respiratory epithelium is pseudostratified ciliated columnar epithelium. Seromucous glands provide lubricating mucus.

 

 

Figure 7 (a) – Represents alveolar exchange of gases in the human lungs.

 

External Respiration In external respiration, oxygen diffuses across the respiratory membrane from the alveolus to the capillary, whereas carbon dioxide diffuses out of the capillary into the alveolus.
Figure 7 (b) – External Respiration In external respiration, oxygen diffuses across the respiratory membrane from the alveolus to the capillary, whereas carbon dioxide diffuses out of the capillary into the alveolus. 

 

Figure 7 (c) – Internal Respiration Oxygen diffuses out of the capillary and into cells, whereas carbon dioxide diffuses out of cells and into the capillary.

 

Figure 7 (d) – Carbon Dioxide Transport Carbon dioxide is transported by three different methods: (a) in erythrocytes; (b) after forming carbonic acid (H2CO3 ), which is dissolved in plasma; (c) and in plasma.

 

Figure 8 – Normal Inspiration and Expiration Inspiration and expiration occur due to the expansion and contraction of the thoracic cavity, respectively.

 

Figure 9 – Intrapulmonary and Intrapleural Pressure Relationships Intra-alveolar pressure changes during the different phases of the cycle. It equalizes at 760 mm Hg but does not remain at 760 mm Hg.

 

 

 

Figure 10 – Respiratory Volumes and Capacities These two graphs show (a) respiratory volumes and (b) the combination of volumes that results in respiratory capacity.

Figure 11 – Respiratory centres of the brain that control the respiratory rate and ventilation. The major brain centers involved in pulmonary ventilation are the medulla oblongata and the pontine respiratory group.

Figure 12 (a)- For practice purposes; represents the respiratory system consisting of the airways, the lungs, and the respiratory muscles that mediate the movement of air into and out of the body.

 

 

Figure 12 (b) – For practice purposes; represents the respiratory system consisting of the airways, the lungs, and the respiratory muscles that mediate the movement of air into and out of the body.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

2 –  Diagnostic Tools – Spirometry, Arterial Blood gas, Oximeter, Exercise Tolerance Testing, X-ray, Bronchoscopy, Culture and Sensitivity Tests, Sneezing Reflex, Coughing Reflex,

 

Figure 1 (a) – An illustration depicting an incentive spirometer.
Figure 1 (b) – An illustration depicting an incentive spirometer.

 

Figure 1 (c) – Flow-Volume Loop. Positive values represent expiration, negative values represent inspiration. The trace moves clockwise for expiration followed by inspiration. (Note the FEV1, FEVA1/2 and FEV3 values are arbitrary in this graph and just shown for illustrative purposes, they must be recorded as part of the experiment).

 

Figure – 2 (a) A medical illustration depicting CO2 & pH.

 

Figure 2(b) – Difference in hue between arterial (brighter) and venous (darker) blood

 

Figure 3 (a) – Representing finger pulsoximeter

 

Figure 3 (b) – Representing Hospital Pulse Oximeter

 

Figure 3 (c) – Representing the working mechanism of the pulse oximeter

 

 

Figure 3 (d) – Simplified principle of operation of a transmissive LED pulse oximetry device
                                                       Figure 3 (e) – Adult reusable fingertip pulse oximeter probe correct placement
                                         Figure 3(f) – Adult reusable hardshell pulse oximeter probe (correct placement) on hand.

 

 

image
X-ray
Figure 4 (a): x-ray tech collimating and correctly positioning a patient for a chest x-ray examination
Figure 4(b): Normal chest X-ray of an adult man

Figure 4(c): Working of an X-ray

Figure 4(d): X-ray Body in Motion – Yoga by Hybrid Medical Animation

 

                                                 Figure 4(e): Chest radiograph with signs of congestive heart failure

 

 

Figure 5(a) – Bronchoscopy (I recreated this using Bio-render)

 

Figure 5(b)- Physicians using a bronchoscope which is a flexible tube with a light inside and is inserted into the patient’s trachea. Doctors can view inside the body through the tube allowing easier access to removal of tumors.

 

Figure 6(a) – Amylase culture and sensitivity tests

 

Figure 6(b) – Staphylococcus aureus culture and sensitivity tests.

 

Figure 7 (a) – reflexes are automatic, subconscious response to a stimulus.

 

Figure 7(b) – Sneezing reflux is a semi-autonomous, convulsive expulsion of air from the lungs through the nose and mouth.

 

Figure 8(a) – Cough can be referred to as a medical symptom, reflex to clear large breathing passages

3 – Signs & Sympoms: sputum (yellow, green, red, rusty, thick tenacious), hemoptysis, breathing sounds and pace, eupnea, laboured, wheezing stridor, rales, rhonchi, absence, dyspnea, orthopnea, cyanosis, pleuritic pain, friction rub, clubbed fingers

 

Figure 1 (a)- Changes in the sputum (phlegm) thickness, color or quantity could be a sign of a health problem like a respiratory infection or lung disease (created using Bio-render).

hemoptysis – is a medical term for coughing up blood from airways or lungs. It is different from vomiting blood or bleeding from nose or mouth. Blood coughed up due to haemoptysis will likely be frothy and bright red. The symptoms include but not limited to fever, fatigue, chest pain, weight loss and shortness of breath.

breathing sounds and pace –

eupnea – also known as quiet breathing or the resting respiration is the normal breath. Here the process is completely passive and engages the elastic recoil of the lungs. In comparison to eupnea, apnea is the absence of respiration, dyspnea is diffcult respiration, bradypnea is slower respiration, and trachypnea is fast respiration.

laboured – is abnormal respiration identified as struggling to breathe. It at times can be accompanied with wheezing or gasping symptoms. The causes for laboured breathing can be many including but not limited to emphysema, lung cancer, tuberculosis, asthma, ventricular dysfunction etc.

wheezing stridor– is a high pitched noise caused due to obstruction around the voice box. To determine the level of obstruction it is important to identify whether the stridor is occurring during the inspiration or the expiration of the breath or both. Its causes could be infection, narrow airways (birth defect), abnormal swelling of the airway or a growth causing the obstruction, compression from external structures, etc.

rales – are the crackling or rattling sounds made by the lungs during inhalation and are caused by the “explosive” opening and collapsing of the small airways due to either excess fluid or lack of aeration. The causes of rales could be atelectasis, pneumonia, congestive heart failure etc.

rhonchi – is an involuntary and abnormal sound heard caused usually due to secretions obstructing the airway passage. The sounds are caused by the air forcefully flowing through the thick mucus secretions deposited in the larger as well as the smaller airway structures like bronchioles and alveoli. It is the mostly common in COPD and bronchitis patients.

absence – 

dyspnea – it is an uncomfortable breathing sensation. It involves different shortness of breath sensations, including but not limited to suffocation, chest tightness, partial exhalation, gasping/hunger for air, shallow, fast and heavy breathing. The common dyspnea causes are heart failure, pulmonary edema, pneumonia and pregnancy.

Figure 2(a) – Shortness of breath
Figure 2(b) – Shortness of breath

orthopnea – is dyspnea occurring lying flat. When a orthopnea patients lies flat there is an increase in venous return to the lungs that causes an increase in venous and pulmonary pressure. It stops the patient from lying normally and to sleep sitting-up. It can be commony seen in asthmatic, bronchitis, sleep apnea or heart patients.

Figure 3 – Heart failure

cyanosis– occurs when there is oxygen shortage in the blood. The inadequate oxygen causes the skin, lips, earlobes and nails to turn blue-purple tint. It is usually caused by heart, lungs or blood-related issues.  

Figure 4(a) – Local hypxia
Figure 4(b) – Cyanotic neonate
Figure 4(c) – Cynosis
Figure 4(c) – Dependent Acrocyanosis in a Norwegian 33-year old male POTS patient
Figure 4(d) – Arterial thrombosis causing cyanosis
Figure 4(e) – Lifelong cyanosis and skin color and arterial blood color in the patient’s family.

pleuritic pain– is caused during pleurisy, a condition of inflamed pleura caused by a variety of virus or bacterial or other illnesses that travels to the pleurae. The pleuritic chest pain can be defined as a sharp pains that gets worse during inspiration or expiration. Apart from the bacterial or viral infections, pleurisy can also be caused by autoimmune diseases (lupus), pleural disease (i.e., mesothelioma), chest trauma, sickle cell disease, IBD, pulmonary embolism and certain medications etc.  (can make an image using bio-render)

friction rub – also known as pleural friction rub, is an involuntary breath sound resulting from the movement of inflamed and swollen pleural surfaces against each other. It can usually better heard during lung auscultation.

Figure 5(a) – Pleurisy

 

Figure 5 (b)- Fibrinous pleuritis

clubbed fingers – also known as clubbing is a finger deformity associated with heart or lungs diseases involving constant low oxygen levels. Here, the angle of nail bed gets distorted, fingernails enlarge and get really curvy. The most common cause of clubbed finger is lung cancer however it can also be caused by heart defects, heart/lung infections, celiac disease, cirrhosis etc. 

Figure 6 (a) – clubbed fingers

 

Figure 6 (b) – clubbed fingers
Figure 6 (b) – clubbed fingers (showing the change in the angle of nail bed)

4 – Definitions: hypoxemia, hypercapnea, hypoxia, (an informative/summary figure can be made using Bio-render)

 

Diaphragmatic breathing
Figure 1 (a) – diaphragmatic breathing

 

Figure 1 (b) – The muscles used during forceful breathing. Inhalation on the left, exhalation on right. Contracting muscles are shown in red. Relaxing muscles are in blue.

Hypoxemia – is a condition involving abnormally low blood oxygen levels. It can lead to bluish skin, difficulty breathing and fast heart rate. Apart from sleep apnea and higher altitudes, hypoxemia can be also be caused by many underlying illnesses, mainly lung and heart related especially in conditions of low environmental oxygen, diffusion impairment, hypoventilation, right -to left atrial shunting (image below).

Figure 2 (a) – Oxygen-Hemoglobin Dissassociation Curve.

 

Figure 2 (b) – Right -to left atrial shunting – Atrial septal defect (ASD) is a form of congenital heart defect that enables blood flow between the left and right atria via the inter-atrial septum.

Hypoxia – is a condition involving abnormally low levels of oxygen in body tissues. It can lead to bluish skin, confusion, difficulty breathing, restlessness and fast heart rate. Hypoxia is different to hypoxemia as hypoxia is low oxygen levels in tissues whereas hypoxemia is low oxygen levels in blood.

Figure 3 (a) – video – https://commons.wikimedia.org/wiki/File:Hypoxia_video.webm#file (unable to address citations for this video)

Figure 4 (b) – Hypoxia

 

Figure 4 (c) – Tissue shows higher level of expression in hypoxic situations.

 

Figure 4 (d) – How Cells Sense and Adapt to Oxygen Availability. Under normoxic conditions, Hif-1 alpha is hydroxylated at two proline residues. The protein then associates with VHL and is subsequently tagged with ubiquitin. Tagged Hif-1 alpha is then translocated to the proteasome, where it is degraded. Under hypoxic conditions, no oxygen is available for proline hydroxylation. In this situation Hif-1 alpha translocates to the cell nucleus and associates with Hif-1 beta, also termed ARNT. This complex then binds to a DNA region termed HRE (hypoxia responsive element). As a consequence target genes are transcribed. These genes are involved in the regulation of a multitude of processes, including erythropoesis, glycolysis and angiogenesis.

 

Figure 4 (e) – Muscle pathways during Contraction/Hypoxia

 

Figure 4 (f) – During Hypoxia, as a response to stress signal, the p53 protein is activated by post-translational modifications – pathways of the p53 protein.

 

Figure 4 (g) – Hypoxia leads to EMT (epithelia-mesenchymal-transition) (couldn’t find a better resolution for this one)
Figure 4 (h) – MAYBE TOO MUCH INFOR (added just incase)- Methylation status and 5hmC levels in normal, tumor, and hypoxic tumor cells. In normal cells, particularly in ES and hematopoietic cells, TET proteins are highly abundant, usually in accordance with an enrichment in 5hmC and unmethylated DNA (white circle). However, during tumorigenesis, many of the CpG islands near or around the promoters of tumor suppressors are highly methylated (dark circle). Loss of 5hmC and TET proteins can be detected globally or site-specifically. However, when tumor cells undergo hypoxia, TET proteins can be induced by HIF-1α and elevated 5hmC composition can be detected at promoters, introns, exons, as well as 3 1-UTR at a global scale (76), leading to gene expressions, e.g., those in the EMT and metabolic pathways. Hypoxic tumor cells are thus more malignant with enhanced migration/invasion, angiogenesis, and stemness, etc., and resistant to anti-cancer drugs.
TSS: transcriptional start site;
TTS: transcriptional termination site

 

Figure 4 (i) -CT in a person after generalized hypoxia.

 

Figure 4 (j) -Profound hypoxia – Computed tomography of the skull in a patient after generalized hypoxia: The metabolically intensive and therefore hypoxia-sensitive regions such as the globus pallidum, hippocampus and the cerebral crura are particularly affected. The medulla-cortical differentiation is also significantly reduced.

 

Figure 4 (k) -Hypoxic Training Index graph explaining how hypoxia dosage delivered during Intermittent hypoxia therapy or training (altitude training) is calculated.

Hypercapnea – is also known as hypercarbia. It is a condition related to high carbon dioxide levels in the body. Carbon-dioxide can get built up in the blood if the body doesn’t successfully get rid of it within time. Conditions that either increase the levels of carbon-dioxide in the body or prevent the waste carbon-dioxide from getting to the lungs and discarded are usually the main causes of hypercapnea. Illnesses related to lung, brain, muscles and nerves are usually the most common causes. Hypercapnia is different to hypoxemia as hypercapnia is the condition with high carbon-dioxide levels in blood whereas hypoxemia is low oxygen levels in blood. 

 

Figure 5 (a) – Oxygen-Haemoglobin dissociation curves

 

Figure 5 (b) – Main symptoms of carbon dioxide toxicity, by increasing volume percent in air.

 

Figure 5 (c) – Sleep state-related ventilation in an 8-year-old boy suffering from congenital central hypoventilation syndrome (CCHS): Severe hypercapnia during deep NREM sleep, normocapnia during REM sleep. An increased FiO 2 kept the PO 2 at normal values.

 

Figure 5 (d) – Hyperventilation is increased airflow in lung alveoli due to fast or deep breathing, while Hyperpnea describes breathing that is more rapid and deep.

5 – Aging Respiratory System – arthritic changes, emphysema, elastcitiy (compliance) (an informative/summary figure can be made using Bio-render)

– I am not sure if this is what exactly is needed here, but I added what I thought was relevant to the topic. 

Arthritic changes – Arthritis is related to a condition of painful joints due to inflammation or swelling. A type of arthritis is rheumatoid arthritis, it is an autoimmune disease where the immune system attacks the joints, starting with the lining of joints. Rheumatoid arthritis is heavily related to lung problems, about 80% of arthritic patients have lung-related issues, making it the second leading cause of death with rheumatoid arthritis patients. Rheumatoid arthritis caused lung problems are most commonly extra-articular  i.e., outside of the joints and involves pulmonary nodules; damage to the lung airways, pleural effusion and interstitial lung disease. In rheumatoid arthritis associated interstitial lung disease the auto-immune system gets over active and attacks the lungs and causes scarring. With time, the scarring build-up leads to difficulty breathing and reduced lung function.

 

Figure 1 (a) – Osteoarthritis and rheumatoid arthritis – Normal joint Osteoarthritis Rheumatoid arthritis

 

Figure 1 (b) – Normal vs Osteoarthritis
Figure 1 (c) – Normal Joint Vs Rheumatoid Arthritis
Figure 1 (d) – Normal vs Rheumatoid arthritis joint

 

Figure 1 (e) – Effects of chronic rheumatic arthritis

 

Figure 1 (f) – Osteoarthritis of a synovial joint results from aging or prolonged joint wear and tear. These cause erosion and loss of the articular cartilage covering the surfaces of the bones, resulting in inflammation that causes joint stiffness and pain.

 

Figure 1 (g) – Magnetic resonance images of fingers: psoriatic arthritis. Shown are T1-weighted (a) precontrast and (b) post-contrast coronal magnetic resonance images of the fingers in a patient with psoriatic arthritis. Enhancement of the synovial membrane at the third and fourth proximal interphalangeal (PIP) and distal interphalangeal (DIP) joints is seen, indicating active synovitis (large arrows). There is joint space narrowing with bone proliferation at the third PIP joint and erosions are present at the fourth DIP joint (white circle). Extracapsular enhancement (small arrows) is seen medial to the third and fourth PIP joints, indicating probable enthesitis. Note that this particular slice does not allow optimal visualization of all of the mentioned pathologies.
Figure 1 (h) – Signs of destruction and inflammation on ultrasonography and MRI in second metacarpophalangeal joint: established RA. Thin arrows indicate an erosive change; thick arrows indicate synovitis. Ultrasonography in the (a) longitudinal and (b) the transverse planes shows both signs of destruction (grade 2) and inflammation (grade 3). Axial T1-weighted magnetic resonance images were obtained (c) before and (d) after contrast administration (grade 3 synovitis). Additionally, a coronal T1-weighted magnetic resonance image (e) before contrast administration visualizes the same bone erosion as shown in panels c and d. The coronal magnetic resonance image of the second metacarpophalangeal joint (panel e) is additionally covered by a grid illustrating division of the assessed joints into quadrants: proximal radial, proximal ulnar, distal radial and distal ulnar. MRI, magnetic resonance imaging; RA, rheumatoid arthritis.

 

Figure 1 (i) – X-ray of rheumatoid arthritis of the shoulder of a 28 year old woman. There are numerous periarticular joint erosions (arrows) and joint space narrowing which is consistent with diagnosis of with rheumatoid arthritis.

 

Figure 1 (j) – Rheumatoid arthritis of the hand

 

Figure 1 (k) – Hemothorax complicating rheumatoid arthritis

 

Figure 1 (l) – Autoimmune Disorders (a) Rheumatoid Arthritis and (b) Lupus (couldn’t crop out lupus part out of this image)*

 

Figure 1 (m) – A hand severely affected by rheumatoid arthritis.

 

Figure 1 (n) – Ankle Joint Arthritis

 

Figure 1 (o) – Swan neck deformity in a 65 year old Rheumatoid Arthritis patient

 

Figure 1 (p) – Follicular bronchiolitis may be associated with a variety of conditions including collagen vascular diseases, immunodeficiency syndromes, hypersensitivity reactions, bronchiectasis, obstructive pneumonia and chronic infections.In this individual the lesion is associated with rheumatoid arthritis and bronchiectasis. It is characterized by the presence of lymphoid folllicles with germinal centers involving the wall of a bronchiole.
Figure 1 (q) – Here the lesion is associated with rheumatoid arthritis and bronchiectasis.

 

Figure 1 (r) – Follicular bronchiolitis associated with bronchiectasis and rheumatoid arthritis

 

Figure 1 (s) – Follicular bronchiolitis associated with bronchiectasis and rheumatoid arthritis

 

Figure 1 (t) – Gold is an effective agent for controlling some types of arthritis, especially rheumatoid arthritis. It can either be injected into a muscle in the buttock or arm or be taken orally in capsule form. Injected gold is generally more effective than gold taken orally. It is usually given as gold sodium thiomalate (brand name: Myochrysine®) or as aurothioglucose (brand name: Solganal®. In capsule form gold is given as auranofin (brand name: Ridaura®). In this case the gold was likely injected into the upper arm and some then drained to axillary lymph nodes.

 

Figure 1 (u) – Symptoms used to assess the presence and degree of arthritis

 

Figure 1 (v) – Venn diagram for type of pain and chronicity. Pain from a minor foot sprain would be considered normal and nociceptive because it is signaled by tissue injury (i.e., a normal mechanism). Inflammatory pain from arthritis (center) is an example of a nociceptive mechanism because inflammation is the cause of pain. Inflammation is also pathophysiologic because it involves an altered (i.e., disease) state. NP is at the right, considered only as pathophysiologic because pain is elicited by abnormal pain mechanisms. Normal pain is only acute, whereas inflammatory or NP may be acute or chronic.

 

Figure 1 (w) – Hypothetical contribution of EMT-like process to the pathophysiology of RA (Rheumatoid Arthritis). Upon stimuli such as inflammation (IL-1β, TNF-α and IL-17) or hypoxia, several signaling pathways become activated in normal FLS present in the synovial lining. (this is the highest resolution i can find for this image; I can remake it in bio-render – if you’d like this image in the book)

 

Figure 1 (x) – Illustration showing proposed common mechanisms of local inflammation in RA-related membrane involvement including similarities in the development of synovitis, pleural and pericardial effusion, and meningitis.

 

Figure 1 (y) – Prevalence of evaluated comorbidities in the 3920 patients with rheumatoid arthritis.

Emphysema – With age there are various structural, functional and immunological changes that take place within the respiratory system. The anatomical changes include thoracic spine and chest wall distortion leading to impairment in the respiratory system and heavier breathing load. Due to the loss of its supporting structures, the lung parenchyma faces “senile emphysema” i.e., dilation of air spaces.  In addition to that, the airway clearance needed for effective cough is also hindered due to the loss of strength in the respiratory muscles.

Elastcitiy (compliance) – Aging is strongly associated with a significant decrease in elastic recoil and fibrous strength. With age, there is inevitable reduction in the thoracic compliance and augmentation in lung compliance. Thoracic (chest wall) compliance regulates the elastic load during inhalation whereas the lung compliance regulates the rate and force of exhalation. With aging there are significant structural changes to the thoracic spine and cage which ultimately leads to depletion in chest wall compliance.

6. Acute Respiratory Distress Syndrome (ARDS)

For distinction from neonatal respiratory distress syndrome, acute respiratory distress syndrome was also labelled as adult respiratory distress syndrome (ARDS). It involves inflammation in the lung parenchyma, increased alveolar permeability, reduced lung compliance and non-functional gas exchange. The increased alveolar permeability allows fluid to build up which in-turn prevents the lungs from filling up air, causing less oxygen in the bloodstream. The oxygen deprivation sequentially leads to organ failure. Low blood-oxygen levels in the bloodstream not only affects the lungs but, also harms other organs in the body and prevents oxygen from reaching them for normal functioning. The intensity of the disease can be determined by measuring and comparing blood-oxygen levels. ARDS is a rapidly developing and potentially fatal lung disease, most people don’t survive ARDS. ARDS survivors mostly have lasting damage to their lungs. The risk of death and the severity of the disease increases with age. The main symptom of ARDS is distressing shortness of breath, which develops within the first couple hours and lasts longer than the illness and the duration of recovery.

7. Respiratory Failure

Respiratory failure is a critical condition that develops due to low blood-oxygen levels in the bloodstream that makes involuntary tasks like breathing almost impossible to do on your own. The low blood-oxygen levels results due to inadequate gas exchange during pulmonary circulation, which could be because of pump failure or lung failure. Pump failure is a ventilation failure which causes hypercapnia whereas lung failure is gas exchange failure causing hypoxemia. It can also de defined as arterial oxygen tension (Pao2 < 60mmHg) or arterial carbon dioxide tension (PaCO2).

 

Inverse relationship between the partial pressure of carbon dioxide and plasma pH

Respiratory failure can be of four types depending on their intensity levels;

Type I: – involves a ventilation/perfusion mismatch that causes untreatable hypoxemia (PaO2). Another characteristic of type I respiratory failure is alveolar flooding.

Type II: – involves alveolar hypoventilation resulting in hypercapnia (PaCO2). There is a significant reduction in the alveolar minute ventilation that entails inadequate removal of carbon dioxide.

Acute respiratory failure vs chronic respiratory failure: In type II respiratory failures, there is active vs chronic respiratory failure, active failure matures and progress over minutes to a couple days and involves respiratory acidosis (a condition where lungs are not able to get rid of all the carbon dioxide in the body). On the contrary, chronic failure takes anywhere from days to months to develop and involves a higher PaCO2 including increased levels of serum bicarbonate due to renal compensation.

Type III: – type III respiratory failure usually takes place in the peri or post operative period where the abdominal wall mechanics are abnormal. Patients usually have progressive atelectasis due to inadequate functional residual capacity leads to . The clinical progression of type III respiratory failure usually leads to either type I or type II respiratory failure.

Type IV: – is due to underlying circulatory collapse or shock (insufficient oxygen levels in the body) due to which patients are usually mechanically ventilated.

 

Types of Respiratory Failures

Causes of Respiratory Failure:  can occur due to issues in any pathological or anatomical parts of the respiratory system.

  • Central Nervous System – any condition that affects or lowers the conscious level.
  • Peripheral Nervous System – any condition that affects the peripheral neural system (e.g. Guillain-Barré syndrome (GBS), nerve or spinal injury)
  • Musculoskeletal System – any condition that affects the musculoskeletal part of the body (e.g. rib fractures, neuromuscular blockade)
  • Airway Pathology – any condition that affects the airways (e.g. tumor, foreign body or laryngospasm)
  • Pleural Pathology –  any condition that affects the pleural parts of the lungs (e.g. haemothorax, pneumothorax or effusions)
  • Pulmonary Pathology – any condition that affects the lungs (e.g. pulmonary fibrosis, pulmonary oedema, ARDS)
  • Vasculature – any condition that affects vascular parts of the lungs (e.g. pulmonary embolism)
A – location of the lungs, airways, diaphragm, rib cage, pulmonary arteries, brain, and spinal cord in the body.
B – shows the major conditions that cause respiratory failure.

Assessment/diagnosis: There are specific tests that can be done for diagnosis and advising the right therapy:

  • Chest X-ray – can be used to image any problems or abnormality in lung pathology (e.g. pleural effusions etc).
Chest radiograph with signs of congestive heart failure
  • Computed Topography – can be used for an intensive and more detailed imaging of injuries and abnormalities in the anatomical pathology (e.g. detection of pulmonary emboli or airway tumor).
  • Arterial Blood Gas – this test can be done for quantifying the severity of the respiratory failure or measuring the oxygen concentration in the blood to test for hypoxia severity.

 

Arterial blood gas device

 

Cobas b 121 (Roche Diagnostics) – measurement chamber (detail). From the left: Reference electrode, Sample’s conductivity electrode, Na+ electrode, Cl- electrode, pH (glass) electrode, Sample’s conductivity electrode, Ca2+ electrode, K+ electrode, pO2 (Clark) electrode, (pCO2) (Sveringhaus) electrode, Hemoglobin/Hematocrit chamber.
Impact of arterial blood gases on alveolar ventilation
  • Peak Expiratory Flow – this test can be done to measure the severity of airway obstruction.

 

Normal values for Peak Expiratory Flow PEF – EU scale – symbolic designators.

 

Peak Flow Meter as issued by an NHS doctor ın the UK

 

Two Peak Flow Meters
A child using a peak expiratory flow meter in a pediatric clinic.
  • Thoracic Ultrasound – this test is superior to any other tests in determining the respiratory conditions.

Management: Like any other acute disease management, management for respiratory failure should also start with general measures leading up to the more focused strategies depending on the type and severity of the condition.

General Measures:

  • Supplemental Oxygen – usually indicated for majority of the patients, can be delivered using devices such as nasal cannulae or Venturi masks.
Nasal Cannula
Nasal prongs/ cannula 
Simple face mask/ Venturi masks
Venturi Masks
  • Secretion Control – In patients with respiratory failure there is often high production of sputum secretions that can cause poor gas exchange and lead to mucus plugging or lung failure. To prevent this from happening simple strategies like deep breathing, chest physiotherapy or mucolytic medications can help.
  • Antibiotics – can and should only be taken if there is an infection and within the hour of diagnosis.
  • Bronchodilators – are generally offered and provided to patients with substantial airflow obstruction to reduce airway inflammation and narrowing.
    Bronchodilators

Specific Measures: are only really applied if any improvements are seen through the general measures.

  • High flow nasal cannulae – consists of wider – bore prongs and offers humidification and titration of oxygen concentrations to be delivered.
Sketch of heated humidified high-flow therapy
  • Continuous positive airway pressure (CPAP) – machine supplied continuous positive pressure during the entire breathing cycle causing better oxygenation by narrowing the shunt (i.e., inadequate alveolar ventilation). This is generally using in high dependency units.
CPAP continuous positive airway pressure mask installed

 

CPAP Therapy Device

 

Depiction of a Sleep Apnea patient using a CPAP machine

 

Premature in incubator with CPAP
  • Non-Invasive Ventilation – helps with the supply of bi-level positive airway pressure. This can be provided using simple or more sophisticated machines outside or inside high dependency units, respectively. It is one step down from invasive ventilation strategies.
Patient wearing a non-invasive ventilation mask.
Non invasive ventilation
Non invasive ventilation
BiPAP using a ventilator
  • Invasive Mechanical Ventilation – here a tracheostomy (insertion of a tube into the trachea from outside) is performed. It is only applied when the rest of the measures have failed (i.e.,  CPAP or NIV fails; deteriorating blood gases despite focused medical treatments) or conditions such as, clinical deterioration, sever respiratory acidosis or muscle fatigue. There are very high risks and complications of invasive mechanical ventilation and therefore it is only commenced in special cases and alway by a intensivist/specialist.
Figure A shows a side view of the neck and the correct placement of a tracheostomy tube in the trachea, or windpipe. Figure B shows an external view of a patient who has a tracheostomy.
Schematic cross-section representation of a tracheotomy numbered 1-5 indicting different features of the anatomy:
vocal cords:
1- Thyroid cartilage
2- Ring corpel
3- Tracheal cartilage
4- Balloon cuff

 

Tracheostomy tubes.
Diagram showing a fenestrated and a non fenestrated tracheostomy tube
A tracheal stoma after a total removal of the larynx.

 

Tracheostoma

 

Flowchart describing use of noninvasive ventilatory support (NVS) in acute care setting for patients with ventilatory pump failure. NVS settings refer to pressure spans of at least 18 cm H2O with no supplemental oxygen, while MIE should be performed at 50-60 cm H2O. BiPAP devices may also provide NVS at those settings with expiratory positive airway pressure minimized if a portable ventilator is not available. CNVS = continuous noninvasive ventilatory support, MIE = mechanical insufflation-exsufflation, BiPAP = bilevel positive airway pressure.

 

8. Cystic Fibrosis :

Symptoms of Cystic Fibrosis

 

  • before you start cystic fibrosis – add figure legend for all the images you added

  • double check images for before respiratory failure  – add ones you forgot

  • add non-invasive images too

  • block the parts you’ve concluded

  • START FROM HYPOXIA PARAGRAPH.

 

 

 

  1. Cystic Fibrosis
  2. Lung Cancer
  3. Allergies,
  4. Asthma – Extrinsic and Intrinsic
  5. COPD – Emphysema
  6. COPD – Chronic Bronchitis
  7. Pulmonary Embolus
  8. Ventilation:Perfusion ratio/shunt
  9. Atelectasis – obstructive, compression, contraction, postoperatvive
  10. Pleural effusion
  11. Pneumothorax – closed (simple/primary or secondary), open, tension
  • NEED TO GO BACK AND CHECK OPEN-STAX AND OTHER RESOURCES FOR ALL THESE TOPICS

Sakshi – It looks like we can’t embed Sketfab – as shown by large gray boxes below, but we can insert hyperlinks to their website… I’ve started doing this for you. (click on open in new tab)..

From Sketchfab, try out:

  1. 3D Labelled Anatomy of the Larynx
  2. 3D Labelled Respiratory System part 1
  3. 3D Labelled Respiratory System part 2

 

 

Respiratory System 1 by DrB1000 on Sketchfab

Respiratory System 2 by DrB1000 on Sketchfab

 

Respiratory System Unlabeled by DrB1000 on Sketchfab

Anatomy Of The Larynx by DrB1000 on Sketchfab

Respiratory Sys Detail by DrB1000 on Sketchfab

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The next one is from: https://sketchfab.com/3d-models/pathophysiology-of-asthma-6d215eab5a324f4ca8ed74c3db36aa87

Pathophysiology of Asthma by N351SON on Sketchfab

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Chapter 6 Respiratory Diseases and Disorders - Sakshi Copyright © by Zoë Soon is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License, except where otherwise noted.

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