Week 1

On the first of February, 2016 we had our first lecture for BEH2432. Since we did not have any practical session in the first week, there will be no reflection in this entry.

Learned Concepts

The airway includes the following structure in this order: Nose, nasopharynx, oropharynx, epiglottis, laryngopharynx, vocal cords, larynx, trachea, carina, bronchi, bronchioles (Terminal then respiratory), alveolar duct, alveoli.
The glottis is a landmark distinguishing between upper and lower airways. Above the glottis is the upper airway and below the glottis the lower airway.
In the airway, the first cartilage is called the thyroid cartilage and the one inferior to it is the cricoid cartilage. Between them is the crico-thyroid membrane. My teacher told us this membrane is where cricothyroidtomy is performed.

Breathing is the movement of air in and out of the lungs. It is possible due to this chain of events:
Respiratory muscles contract/relax -> causes pressure difference -> Air moves from area of high pressure to low pressure (In/ out of lungs)

When the pressure inside the lungs is <760mmHg, Air moves from atmosphere to inside lungs (Where pressure is lower).
This inhalational process is active where the medulla oblongata commands the inhalational muscles to expand the chest and lungs. This increases the volume of the lungs, and according to Boyle's Law, decreases the pressure. This causes air to move into the lungs.
On the other hand, exhalation is passive. This is because it is triggered by the relaxation of the inspiratory muscles. This leads to the chest and lungs recoiling, decreasing the volume of the lungs, which, according to Boyle's Law, increases the pressure inside the lungs to >760mmHg. Air then moves out of the lungs into the atmosphere, where the pressure will be lower.
Between inhalation and exhalation there are moments where the atmospheric pressure equals the pressure in the lungs. Therefore, no air moves in or out of the lungs. This is why the RR is normally 12 breaths per minute, since our bodies are not continuously breathing.

Figure 1: Diagram showing and explaining the two types of respiration

For oxygen, the pressure is higher in alveoli compared to the pressure in capillaries. This is why oxygen moves from the alveoli to the blood in the capillaries.
For carbon dioxide, the pressure is higher in capillaries when compared with alveoli. This is why CO2 moves from capillaries to alveoli during external respiration.
It is important to note that the PaCO2 is equal to 35-40 mmHg.
External respiration and diffusion is effected by:
1- O2 concentration: increased O2 -> increased diffusion of O2 from alveoli to capillaries
2- Altitude: Harder to breathe at high altitudes
3- Loss of lung tissue: Less tissue -> smaller surface area -> decreased diffusion
4- PEEP, CPAP, BIPAP: high pressure-> increase surface area -> increased diffusion

O2 is transported via blood, in internal respiration, by plasma but mostly by binding to hemoglobin.
However, O2 can only enter tissue cells if it is dissolved in plasma. Therefore, dissolved O2 diffuses into the cells, and then hemoglobin bound O2 will dissolve into the plasma, to enter the cell. For this to happen properly, plasma O2 must always be greater than cellular O2, due to the need of a concentration gradient for diffusion to occur.

Conducting airways conduct air to the lungs. No gas exchange occurs in these airways. They begin at the nose and ends at the terminal bronchioles. These airways warm, humidify and clean the air, prevent foreign matter from entering the respiratory airways and serve as a passageway for air to enter the gas exchange regions of the lungs.
These gas exchange regions include the respiratory bronchioles, alveolar ducts, and alveolar sacs.

The main function of the nose relating to the respiratory system is to clean and humidify air on inspiration by action of cilia and conchae.
The pharynx is the common opening to the digestive and respiratory systems. Divided into: nasopharynx, oropharynx, laryngopharynx.
Larynx (voice box) consists of 9 cartilages: 6 paired and 3 unpaired. The most superior cartilage is the thyroid cartilage. The most inferior cartilage is the cricoid cartilage. The third unpaired cartilage is the epiglottis, which prevents any materials from entering the larynx during swallowing, and directs those materials into the esophagus. The larynx contains true and false vocal cords, which vibrate and produce sounds as air moves past them.
The trachea (windpipe) begins at the cricoid cartilage and ends at the carina. Contains smooth muscle and is supported anteriorly by 16-20 C shaped cartilaginous rings.
Thoracic cavity houses and protects most of the lower respiratory system and is flexible enough to accommodate inhalation, where the chest must expand. The thoracic cavity consists of 12 thoracic vertebrae, each with a respective pair of ribs. These provide protection.
Mediastinum is the area between the two lungs and contains the heart, great vessels, esophagus and the lungs' hilum.

The Bronchial tree starts with the left and right bronchi. The left bronchus is narrower than the right one and angles at a 45-55 degree angle. This inclination protects the left bronchus from aspiration. However, due to the angulation and the force of gravity, the right bronchus is the most common site of aspiration and where the ET tube accidentally enters during intubation.
Main stem bronchi are the first generation of bronchi. The final subdivision of the conducting airways are the bronchioles. Bronchioles consist of only smooth muscle!

Figure 2: Drawing of lungs showing structural similarities and differences between right and left lung

Alveoli consist of epithelial cells of types I and II. Gas exchange between the air spaces contained in the alveoli and the capillaries takes place by diffusion across the alveolar capillary walls.

Type I alveolar epithelial cells are squamous cells that compose 90% of alveolar surface, and provide structure for the alveoli. They are the main site of gas exchange and become inflamed when exposed to toxins, making gas exchange harder. This is because the distance the gas has to travel in and out of the alveolar space and capillaries will become larger. 

Within Type I cells there are Pores of Kohn. Also, there are Cannals of Lambert between Type I cells and terminal bronchioles.

Type II Alveolar epithelial cells are cuboidal epithelial cells with microvilli. These cells secrete alveolar fluid which keeps the surface between the cells and air moist. They also produce, store and secrete pulmonary surfactanct, which consists of phospholipids and lipoproteins. Surfactant reduces the surface tension of the alveolar fluid, which reduces the alveoli's tendency to collapse. This fluid also increases lung compliance and eases work of breathing.

Alveolar macrophages are wandering phagocytes that remove fine dust particles and other debris from the alveoli. They move through the Pores of Kohn.

Respiratory membrane (through which gases diffuse): Alveolar wall -> Epithelial basement membrane -> Capillary basement membrane -> Endothelial cells of capillary (Entire membrane= 1/6 diameter of RBC.)

Capillaries allow RBCs to pass through them in a single file. Each RBC is exposed to alveolar gas of two or three alveoli.

Two vascular systems supply the respiratory system:

1- Pulmonary circulation: Pulmonary artery (carrying deoxygenated blood) from rt side of heart -> lungs (gas exchange at alveoli across respiratory membrane) -> Pulmonary vein (carrying oxygenated blood) to lt side of heart -> Systemic circulation

2- Bronchial circulation: Vascular system branching from aorta, that provides perfusion to the tracheobronchial tree. Blood drains into the bronchial veins into the superior vena cava, to return to the heart.

Pleural membranes surround the lungs. Consist of parietal and visceral pleura. 

Parietal -> Attached to thoracic wall

Visceral -> attached to lungs

Pleural fluid is constantly secreted and absorbed. Usually 3-5 mls at any one time. This fluid allows the visceral and parietal pleura to glide against each other during inhalation and exhalation. This fluid is contained in the pleural space.

Within the pleural space there is intra-pleural pressure. Normally intra-pleural pressure is less than atmospheric and intra-pulmonary pressures. Usually intra-pleural pressure is -4cmH2O during exhalation and -10cmH2O during inhalation. 

Intra-pleural pressure results from forces within the chest wall pulling the parietal pleura outwards and elastic fibers within the lungs pulling the visceral pleura inwards. This pressure keeps the lungs inflated. If atmospheric pressure enters the pleural space, such as in pneumothorax, the lung collapses.

The diaphragm performs 80% of work of breathing. The diaphragm separates the thoracic and abdominal cavities and is connected to the sternum, ribs and vertebrae. When it contracts it moves downward, increasing the size of the thoracic cavity -> decreased pressure -> air moves in. In exhalation the diaphragm relaxes, moving upward-> reducing thoracic volume -> increase in pressure -> air moves out.

The diaphragm is controlled by the medulla oblangata via the phrenic nerve (C4). 

Some muscles aid in inhalation and exhalation and these include external intercostals, internal intercostals, scalene, trapezius and sternocleidomastoid. These are called accessory muscles of ventilation. These  muscles enhance chest expansion but are not normally used at rest. If they are used during rest, this is an indication of pulmonary disease.

O2 dissociation curve shows the relationship between dissolved O2, PO2, (x-axis) and hemoglobin bound O2, SpO2, (y-axis). Factors that influence O2 binding including pH, pCO2, Temperature, and 2,3 DPG. Shift to the right means O2 has lower affinity for Hb. Shift to the left means O2 has higher affinity to Hb.
Higher affinity: decreased temperature, decreased 2,3 DPG, decreased [H+], CO poisoning (Hb has higher affinity to Hb -> High SpO2 due to CO binding to Hb, however pt will be hypoxic).
Reduced affinity: increased temperature, increased 2,3 DPG, increased [H+]. 

Ventilation is regulated by:

• A controller within the CNS (Medulla, Pons, Cerebral Cortex [Voluntary])
• Group of effectors (muscles of ventilation)
• Group of central chemoreceptors (Near the medulla oblongata, surrounded by brain ECF)
• Group of peripheral chemoreceptors (Located above and below aortic arch and at bifurcation of common carotid arteries)
• Lung receptors (Stretch receptors located in walls of bronchi and bronchioles and respond to hyperinflation, J receptors and irritant receptors)

Central chemoreceptors respond to changes in hydrogen ion concentration in ECF. High [H+] -> increased ventilation. This is to get rid of excess CO2 which will then reduce the [H+].

Peripheral chemoreceptors respond to changes in PaO2, and increase ventilation in response to hypoxia. Carotid receptors respond to increase PaCO2 and increase ventilation accordingly.

Lung receptors send messages via vagus nerve to the pons to begin expiration, in case of hyperinflation of lungs. This is know as the Hering-Breuer reflex. 

Hering-Breuer reflex: Hyperinflation of lungs -> stretch receptors in bronchi and bronchioles triggered-> signal sent via vagus nerve -> Pons -> Exhalation begins

J receptors are located in alveolar walls close to capillaries. If there is engorgement due to increased interstitial fluid at the alveolar wall, the J receptors stimulate ventilation.

Irritant receptors lie between airway epithelial cells and function to stimulate coughing in response to inhaled irritants.

Figure 3: Diagram showing Respiratory volumes

ABG:

pH: 7.35-7.45 (acid/alkaline)

PO2: 80-100 mmHg (hypoxaemia)

PCO2: 35-45 mmHg (respiratory acidosis/ alkalosis)

HCO3: 22-26 mmol/L (metabolic acidosis/ alkalosis)

Respiratory Status Assessment include:

Position, Patient's appearance, speech, breath sounds, chest auscultation, respiratory rate, respiratory rhythm, breathing effort, pulse rate, skin condition, and consciousness state.

For chest auscultation, ask patient to sit upright and cough, to clear any sputum. Then move diaphragm of stethoscope from apices to bases of lungs. Always compare one lung to the other at the same site on opposite sides. Must ask yourself these questions:

Is there air entry to the bases?

If not where does it differ?

Does left=right?

Are the sounds normal?

Are there any adventitious sounds?

Pulse oximeters are designed to assess only pulsating blood vessels. This is why pulse oximeters can also measure a patient's pulse. However, must always manually check patient's pulse. Pulse oximetry measures the percentage of Hb in arterial blood that is saturated with O2.

Limited in cases of bright ambient light, poor perfusion, venous pulsation, and nail polish.

Asthma can lead to hypoxia, pulmonary hyperinflation (no Hering-Breuer reflex), and hypercapnia (severe acidosis). Hypercapnia is a late stage.
Following the lecture we had a tutorial. In this tutorial we learned about the different respiratory emergencies drugs:
Salbutamol: works on beta-2 receptors causing bronchodilation, without increasing the HR significantly. It is a fast acting, but short lasting  bronchodilator. Other names for it are Albuterol and Ventolin.
Ipratropium bromide: Anti-cholinergic drug causing bronchodilation. Same effect as Albuterol but has a different mechanism of action. It blocks receptors causing brochoconstriction. Another name for it is Atrovent.
Duolin: Ventolin + Atrovent. Double action. Causes bronchodilation and blocks bronchoconstriction. An alternative for this is to mix one vial of each ventolin and atrovent in the nebulizing mask chamber.

Epinephrine: Majorly acts on beta-1 receptors but has alpha receptor effects. Therefore, it increases the heart rate and force of contractility, vasoconstriction and a little bronchodilation. Also called Adrenaline.
Norepinephrine: Primarily acts on alpha receptors and causes vasoconstriction. Also called Noradrenaline.
Dexamethasone: A corticosteroid that maintains bronchodilation. It is also used to reduce bronchial swelling and mucus production. Other names include Solu-cortef and hydrocortisone.
Salmeterol: Slow acting but long lasting bronchodilator. Also called Serevant.
With using nebulizer drugs, usually we add 2mL of normal saline to avoid drying out the patient's mucosa.

Additional Readings

To further understand certain points i found a bit confusing, i conducted a search online and in my textbooks.
For the Pores of Kohn, i was a little lost to what they are. I found that they are the same as the alveolar pores, which connect adjacent alveoli to each other. This allows the air pressure throughout the lung to be equalized. They also provide alternate routes to any alveoli whose bronchi have collapsed (Marieb & Hoehn, 2014). Also, i found out through reading that the intrapleural pressure is negative relative to the intrapulmonary pressure. Therefore, the fluid in the pleural cavity is constantly pumped into the lymphatics. If this is disturbed and fluid accumulates in the pleural cavity, the pressure will become positive.Moreover, any condition that equalizes the intrapleural and intrapulmonary pressures will cause the lungs to collapse. This occurs in pneumothorax (Marieb & Hoehn, 2014).
I wasn't completely sure why breathing is more difficult in high altitudes. Through a literature search, this is what i found:
On sea level, the atmospheric pressure is 760mmHg, which plays a huge role in creating a pressure gradient that leads to breathing. In high altitudes, for example at the summit of Mount Everest, the atmospheric pressure decreases to around 53mmHg (San et al., 2013). This fall in pressure creates complications for the diffusion of air into and out of the lungs. Moreover, this fall in pressure means a decrease in the concentration of the atmospheric oxygen available. This leads to physiological adaptation changes. However, if the pressure changes too quickly, such as in a fest ascend, this can lead to illnesses (Imray et al., 2011).
I also looked up the drugs we discussed in the tutorial in the JRCALC (2013):
Salbutamol is presented as a 2.5mg/2.5mL and is nebulized with 6-8L/min of oxygen. It's use is indicated in patients with acute asthma attack, expiratory wheeze, exacerbation of COPD and as a secondary treatment for patients with shortness of breath due to LVF. There are no contraindications or maximum dose for this drug, however, if COPD is a possible cause then nebulization must be limited to six minutes (JRCALC,2013).
Ipratropium bromide presents as a 250mcg/ 1mL and it's use is indicated in acute severe asthma, acute asthma unresponsive to salbutamol, and exacerbation of COPD unresponsive to salbutamol. It has no contraindications and is nebulized with 6-8 L/min of oxygen. Moreover, in COPD limit nebulization is maximum six minutes. Also, for adults, the maximum dose is 500mcg/2mL (2 nebules) (JRCALC, 2013).
For both of the above drugs, if the patient is in a life-threatening state, time critical transport must be undertaken and nebulization given en route to hospital (JRCALC, 2013).
 Hydrocortisone: It's presented as a 100mg/1mL ampule of hydrocortisone diluted in either sodium succinate or sodium phosphate, or as a 100mg/2mL ampule of hydrocortisone sodium succinate  with water. It's indicated in patients with severe or life-threatening asthma and anaphylaxis. It's contraindicated in patient's that have an allergy to sodium succinate or sodium phosphate. This drug reduces inflammation and suppresses the immune response of the body. In asthma, it will reduc airway edema and mucus production. This drug is usually given through IV as a slow injection over a minimum of two minutes. In adults, the maximum dose is 1 ampule, whether it's the 100mg/1mL or the 100mg/2mL. However, in anaphylaxis, the maximum dose is 200mg/2mL of the 100mg/1mL ampule and 200mg/4mL from the 100mg/2mL ampule (JRCALC, 2013).
Dexamethasone: Presented as a 4mg/mL ampule. Used in moderate and severe croup and it's given via IV but is usually given orally. It's action is that it reduces subglottic inflammation. Usually given as 1 dose (4mg/mL). However, for infants of ages 1 month-12 months are usually given half a dose (2mg/0.5mL) (JRCALC,2013).
Adrenaline: Comes as a pre-filled syringe or ampule as 1mg/1mL (1:1,000) or as a pre-filled syringe containing 1mg/10mL (1:10,000) . It's use is indicated in patient's with anaphylaxis and life-threatening asthma. For patients taking tricyclic antidepressants, hald doses of adrenaline should be administered in case of anaphylaxis. Other than that there is no maximum dose. The usual dose for adults suffering anaphylaxis or life-threatening athma, is 0.5 mg/0.5mL of the 1:1,000 ampule, given every 5 mins (JRCALC, 2013).

Finally, i read some articles that were provided on the Moodle. The following are my notes from those articles:

• Central cyanosis occurs as a result of prolonged hypoxia. It indicates a ventilation perfusion mismatch which implies serious heart or lung disease. This is observed in the lips, oral mucosa, and tongue. On the other hand, peripheral cyanosis indicates vasoconstriction, which could be a physiological or a pathological response (Massey & Meredith, 2010).
• 75% of finger clubbing is associated with pulmonary pathology (Massey & Meredith, 2010).
• When conducting a RSA, we assess the rate, depth and rhythm (Massey & Meredith, 2010).
• Tachypnea in cardiac patients usually indicates moderate to severe cardiorespiratory disease and is an indication of a poor prognosis (Massey & Meredith, 2010).
• Hyperpnea is characterized by rapid and deep respirations (Kussmaul's respirations) and are most common in DKA. These respirations are a compensatory mechanism to blow off excess carbon dioxide in the blood (Massey & Meredith, 2010).
• Hyperventilation there is an increase in both rate and depth. On the other hand, tachypnea there is rapid, but shallow breathing. Cheyne-Stokes respirations gradually decrease and increase in a regular pattern, followed by a period of apnea. Biot's respiration is similar to Cheyne-Stokes respirations, except Biot's is irregular (Massey & Meredith, 2010). 
• Purse lipped breathing is usually seen in patient's with emphysema. This acts a s a physiological PEEP (Massey & Meredith, 2010).
• Expiratory bulging of the intercoastal spaces is common in patient's with a pneumothorax (Massey & Meredith, 2010).
• When auscultating a patient's chest make sure to place the diaphragm of the stethoscope on the patient's bare chest. This is to avoid misinterpreting the rubbing sound of clothes as abnormal breath sounds (Meredith & Massey, 2011).
• Adventitious sounds are extra sounds that are heard over the normal breath sounds. There are three groups: Crackles, wheezes and rhonchi. Wheezes result from air being forced through a narrow airway as a result of swelling and inflammation, usually seen in asthmatic patients. Rhonchi is a lower-pitched wheeze associated with secretions in the large airways, such as in bronchitis. Stridor is a high-pitched wheeze resulting from turbulent airflow in the upper airways. Crackles can be defined as fine or course. Can also be described as early inspiratory, late inspiratory, mid inspiratory, and expiratory (Meredith & Massey, 2011). 

References 

Imray, C., Booth, A., Wright, A., & Bradwell, A. (2011). Acute altitude illnesses. British Medical Journal, 343, 1-10. Doi: 10.1136/bmj.d4943

Joint Royal Colleges Ambulance Liaison Committee. (2013). UK ambulance services: Clinical practice guidelines 2013. Bridgwater: Class Professional Publishing.

Marieb, E.N., & Hoehn, K.N. (2014). The respiratory system. In E.N. Marieb & K.N. Hoehn (Eds.), Human anatomy and physiology (865-913). Essex, England: Pearson Education Limited.

Massey, D.,& Meredith, T. (2010). Respiratory assessment 1:Why do it and how to do it?. British Journal of Cardiac Nursing, 5(11), 537-541. Doi: 10.12968/bjca.2010.5.11.79634

Meredith, T.,& Massey, D. (2011). Respiratory assessment 2: More key skills to improve care. British Journal of Cardiac Nursing, 6(2), 63-68. Doi: 10.12968/bjca.2011.6.2.63

San, T., Polat, S., Cingi, C., Eskiizmir, G., Oghan, F., & Cakir, B. (2013). Effects of high altitude on sleep and respiratory system and theirs adaptations. The Scientific World Journal, 2013, 1-7. Doi: 10.1155/2013/241569

A Standout Moment

I was very confused about about the return of venous blood from the lungs via the pulmonary veins. This is because we always learned that pulmonary veins only carried oxygenated blood. However, now we were learning that it also carried deoxygenated blood and i didn't understand how that is possible. After reading and searching for over an hour online, i have found the answer. Simply, there are multiple anastomoses between the pulmonary and bronchial venous circulations. These anastomoses lead most of the systemic venous blood from the lungs to return to the heart via the pulmonary veins (Marieb & Hoehn, 2014). Therefore, the two venous circulations are linked and that is how deoxygenated blood reaches the pulmonary veins.

Reference

Marieb, E.N., & Hoehn, K.N. (2014). The respiratory system. In E.N. Marieb & K.N. Hoehn (Eds.), Human anatomy and physiology (865-913). Essex, England: Pearson Education Limited.

Biggest Impression

The thing that made the biggest impression on me this week was learning about the cricothyrotomy, since this is an important skill i might learn in the future. Also, learning about the different drugs in the tutorial made a big impression on me, since this directly relates to what i will be doing on the road as a future paramedic.