Week 4

Week 4
Reflection:
Using the Gibb's Reflective Model, i will be reflecting on the practical session we had on the 22nd of February, 2016.

Description: In this week’s practical we were introduced to the equipment needed for IV cannulation. The equipment included: IV cannula, alcohol swab, gauze, sharps box, tourniquet, and film dressing. Our teacher showed us the different gauges of needles and their colors. They are as follows: 14G (orange), 16G (grey), 18G (green), 20G (pink), 22G (blue), 24G (yellow). Also, we learned that when cannulating we must always start distally and then gradually move proximally. This is because fluid will leak into the surrounding tissue if we start proximally then move distally. After this we started practicing how to actually cannulate. After asking for consent, I started by applying the tourniquet to the arm proximally. I then found a good vein, which I was going to cannulate, making sure it was away from the wrist joint. I removed the tourniquet.  After this, I chose my cannula. I picked the 20G and opened the package. Then I began cleaning the site I was going to cannulate with an alcohol swab. I started at the chosen injection site and moved outwards in a circular motion, to clean the surrounding skin. Following this I removed the plastic cover off the cannula and, with the bevel facing upwards, inserted the needle into the skin towards the vein. However, I was not able to get a flashback of blood. I tried around three times until I finally got some flashback. At this moment I pulled the needle out and advanced the catheter further into the vein. I then removed the cap off the needle’s end, and while applying pressure at the proximal end of the catheter, I removed the needle. I then quickly attached the cap onto the end of the catheter. Finally, I applied  the film dressing and marked the date and time of insertion.

Feelings: As we discussed the equipment and process of cannulation I was really interested. When it became my turn to cannulate, I was so excited. I was pretty confident in my ability to do this skill. However, I felt a little disappointed when I was not able to insert the cannula into the vein. It got stressful when I kept trying and it would not work. Nonetheless, when it finally worked, I was pleased with my work. However, I felt that I needed a lot more practice.

Evaluation: Although we briefly learned about IV cannulation in BEH2411, this session was a great refreshing opportunity. Since we did not actually cannulate last semester, this review was great for me to relearn and refresh my memory on the equipment and process of cannulation. I did a good job at preparing the equipment I needed. Also, I asked for consent which is crucial and maintained an aseptic technique, which was great. However, I was not able to insert the cannula into the vein directly. It took me three attempts until I got it correct. This was not good. However, I did, in the end, get the cannula into the vein, which was a positive moment for me. Also, using the film dressing was a really good step to stabilize the cannula. Finally, it was good that I wrote the date and time on the film dressing, in order to have a record of when the cannula was inserted.

Analysis: IV cannulation is a very important skill for me to obtain as a future paramedic. However, as my teacher said, it comes with experience. Only with time and practice I will get better at this skill. Therefore, even though we learned this skill last semester, we did not practice it. This is why it was so important to revise it before we actually do the hands on practice. Having the equipment prepared before starting the procedure is important. This is to have everything within arm’s reach, since this process is risky and can lead to infection. It did not annoy me that much that I did not get the cannula into the vein directly, because as I wrote earlier, I will get better with practice, and this was my first attempt.

Conclusion: In conclusion, I just need to continue revising the details of this skill and practice more and more on cannulation, until it becomes second nature. Other than that I will do everything else exactly the same, since I did a relatively good job.

Action Plan: I plan to memorize the cannula sizes and their colors, since that can come in handy. Also, I plan on continuously practicing performing IV cannulation whenever I get the chance, until I am able to instantly get the cannula into the selected vein. Moreover, I want to try cannulating different veins.

Image 1: IV catheters ordered according to size

Image 2: Equipment needed to perform IV catheterization

Image 3: Me cleaning the selected site or IV catheterization with an alcohol swab

Image 4: Me inserting the IV catheter into the selected vein

Image 5: Observation of flashback

Image 6: Me slowly sliding the needle out of the catheter

Image 7: Me occluding the vein and placing cap at the catheter's end to prevent leaking of blood

Image 8: Me securing the IV catheter with a securing device

Image 9: Patient's hand after completion of IV catheterization

Learned Concepts

Reading the article by Sciurba (2004) gave me a good idea of what we were going to cover in this lecture, chronic obstructive pulmonary disease, and how it differed from asthma.
In this week's lecture we learned about COPD. The following are my notes of what i learned.

COPD is a preventable and treatable disease wiht airflow limitation that can not be fully reversed. This airflow is usually progressive and associated with an inflammatory response of the lungs to noxious particles and gases.
An exacerbation  of COPD is an event  characterized by:

• A change in the patient's baseline dyspnea
• Cough and sputum that is much more than normal in day to day variations
• Acute in onset
• May warrant a change in the patient's regular COPD medications

Exacerbations of COPD are usually precipitated by viruses or bacteria. They are the main cause of acute pre-hospital and in hospital management of COPD patients. Associated with significant morbidity and mortality.

Ranked the third overall burden of disease after heart disease and stroke. Common to be misdiagnosed for asthma or other respiratory problems. Most COPD cases have a history of tobacco smoking (90%).

Image 10: COPD and the disorders within it

85% of COPD patients have chronic bronchitis and 15% suffer from emphysema. Unlike asthma, COPD is chronic and irreversible. 

Risk factors of COPD:

1. Smoking
2. Passive smoking
3. Respiratory infections during childhood
4. Occupational exposure
5. Air pollution
6. Possibly genetic

Obstruction to airflow in COPD is mainly caused by inflammation, that causes scarring and narrowing of peripheral airways and/or destruction of alveoli.

COPD causes problems with gas exchange which cause hypoxia and hypercapnia. Pulmonary hypertension may occur as a late progression of COPD. This is attributed to hypoxic vasoconstriction of small pulmonary arteries (Cor Pulmonale).

Chronic bronchitis is caused by mucous gland enlargement with mucous hypersecretion, smooth muscle hyperplasia, bronchospasm, mucous plugging, cilia lining stops functioning, and bronchial wall thickening.

This leads to loss of supporting alveolar attachments, airflow limitation, airway wall deformation, and airway lumen narrowing.

On the other hand, emphysema is focal destruction of terminal bronchioles and alveoli. Due to a loss of elastin, the walls of alveoli break down, surrounding capillaries are destroyed, and there is mucosal hypersecretion. As emphysema progresses, loss of elastic recoil contributes to airflow limitation. This leads to a significant loss of lung volume. Formation of bullae may lead to spontaneous pneumothorax. This is because coughing causes increased pressure, making the bullae pop. This leads to air moving into the pleurae of the lungs, thus causing pneumothorax.

Image 11: Table of differences between emphysema and chronic bronchitis

Signs of severe COPD exacerbations:

• Use of accessory muscles
• Paradoxical chest wall movements
• Worsening or central cyanosis
• Development of peripheral edema
• Hemodynamic instability
• Cor Pulmonale
• Reduced alertness

Patients may develop cardiomegaly. Rt side of heart has harder time pumping blood to lungs due to pulmonary hypertension. This strains the right side of the heart, leading to Cor Pulmonale.

Signs include rt heart failure, peripheral edema, and JVD. Signs may be evident in ECG with large P waves and RBBB. This is caused because the SA node cannot transmit messages properly, taking atrial depolarization a longer time. These signs in COPD have a poor prognosis.

Assessment of COPD patients should determine the normal status of the disease in the patient and the precipitants of the exacerbation.

Assessment includes:

• SpO2
• Cardiac monitoring
• Temperature
• BP
• Chest auscultation
• RSA
• GCS
• PSA

Must look for increased work of breathing, use of accessory muscles, cyanosis, faitgue, development of pedal edema, change in conscious state. 

DD: Asthma, congestive heart failure, pneumonia, pleural effusion, pneumothorax, pulmonary embolism, cardiac ischemia, arrhythmia, rib fracture, upper airway obstruction.

Ambulance management similar to that of asthma. Focus is on rest, reassurance, oxygen administration, inhaled bronchodilators (beta 2 agonists and anticholinergic nebulization).

The stimulation of breathing is normally in response to hydrogen ion accumulation in the CSF. As PCO2 increases, hydrogen ion concentration also increases. In end stage COPD patients CO2 levels and hydrogen ion concentration are chronically high. Chemorecptors then reset their tolerance or threshold levels for CO2, this leads to the body becoming desensitized to CO2. Instead of relying on CO2 to stimulate breathing, the body now responds to falling O2 levels as a stimulant. Therefore, if the patient is administered high-flow oxygen, PaO2 will rise significantly, removing the stimulus to breathe.

When giving a COPD patient O2, monitor closely!!!

Reference

Sciurba, F.C. (2004). Physiologic similarities and differences between COPD and asthma. Chest, 126, 117-124. doi: 10.1378/chest.126.2_suppl_1.117S

Additional Readings

To further understand the drugs i learned last week, and more drugs and treatments used for asthma and COPD and their actions, i read the following pages in my textbook:

Image 12: Highlighted notes about initial management of a dyspnea patient such as in COPD and asthma. Adopted from (Moore, 2013).

Image 13: Highlighted notes about intubation and metered dose inhalers. Adopted from (Moore, 2013).

Image 14: Highlighted notes on MDI, aerosol therapy, and dry powder inhalers. Adopted from (Moore, 2013).

Image 15: Highlighted notes on SC, direct instillation, fast and slow acting bronchodilators. Adopted from (Moore, 2013).

Image 16: Highlighted notes about drugs used to treat asthma symptoms and their actions. Adopted from (Moore, 2013).

Image 17: Highlighted notes about vasodilators and CPAP. Adopted from (Moore, 2013).

Image 18: Highlighted notes on BiPAP and automated transport ventilators. Adopted from (Moore, 2013).

Following this i opened my JRCALC(2013) to check what the algorithm for managing a COPD patient was.

Image 19: Assessment and management algorithm for COPD patients. Adopted from (JRCALC, 2013).

I also read an article which was among the recommended readings. This article talked about the delivery of oxygen in COPD patients and how to avoid the hypoxic drive associated with COPD. The main information i gained from this article was that the target SpO2 for a COPD patient must be within the range 88-92%.  This reduced the risk of mortality by 58% (Ntoumenopoulos, 2011).

References

Join Royal Colleges Ambulance Liaison Committee. (2013). UK ambulance services: Clinical practice guidelines 2013(4^th edition). Bridgwater: Class Professional Publishing.

 Moore, S.W. (2013). Respiratory emergencies. In A.N. Pollak (Ed.), Nancy Caroline’s emergency care in the streets(pp.39.27-39.36). Burlington, MA: Jones and Bartlett Learning.

Ntoumenopoulos, G. (2011). Using titrated oxygen instead of high flow oxygen during an acute exacerbation of chronic obstructive pulmonary disease (COPD) saves lives. Journal of Physiotherapy, 57(1), 55. doi: 10.1016/S1836-9553(11)70008-X

Stand Out Moment

This week my stand out moment was when i read the article by Ntoumenopoulos(2011). At first, i did not really understand how the hypoxic drive worked and how i can avoid it. After reading the article it became clear to me that via titrated oxygen delivery i can reduce the effects of the hypoxic drive and save patients in the future. Also, it made sense to target an SpO2 of 88-92%. This is because an increase in the SpO2 beyond this range can stop the body's stimulation for the patient to continue breathing due to the hypoxic drive.

Biggest Impression

 Learning about the assessment and management of COPD patients stood out to me as a future paramedic because this is what i will be applying in my future practice. Learning about the signs and symptoms and how to differentiate emphysema from chronic bronchitis also made an impression on me because this information will help me identify COPD in my practice. Also, it was interesting to me as a paramedic to learn the DD so that i always keep my mind open to the different possibilities as to what my patient is suffering from.