Final

Finally, I will reflect on the process of doing this clinical portfolio, using the Gibb's Reflective Model.

Description: Writing this portfolio has allowed me to really think about my day and how i did and where i need to improve. Also, it really helped me stay up to date with my studies by summarizing every week's lecture. Furthermore, i conducted additional research that really helped me in my understanding of the topics and to widen my learning further than just reading the lectures.

Feelings: I feel so good now that i have finished this portfolio, bu i also feel a sense of loss. This portfolio has been with me throughout the semester and i have grown really accustomed to typing it up.

Evaluation: This whole portfolio has been a GREAT experience and i believe it will really help me in the future with respect to research and really getting the best and total experience from my education.

Analysis: This portfolio has been like a close friend to discuss everything i did and learned during the Wednesdays of this semester. I never really understood reflections, but after this i see how useful and helpful to me they are. They really made me think of everything i did and how i want to improve myself.

Conclusion: I don't know really. I feel like i have put so much effort and time into this portfolio i really can't think of anything other than taking more photos next time!

Action Plan: I plan to do a portfolio for all my subjects with extensive lab training. Also, I plan to study my lectures week by week starting next semester, since this portfolio has shown me how easy and beneficial that is. Furthermore, from now on i will do all my readings since they really do make a difference to my understanding of the subject.

Thank you for reading my portfolio and i hope it was interesting and enjoyable :)

Week 13

Reflection:

Using the Gibb’s Reflective Model I will reflect on the twelfth Lab session we had for this semester. It took place on the 25th of November.

Description: This week we had the insertion of an advanced airway OSCE. I followed the steps in the OSCE marking sheet and answered my examiner’s questions. I passed this OSCE. Later we practiced auscultating different breath sounds on the mannequin. Mine was diminished in the rt lung and normal in the lt. But I got it wrong. After that my colleagues and I prepared our jumpbag for another epic scenario. This time we had everything in the bag so as not to keep running to the store during the scenario. After this my teacher invited my dad to watch me perform an approach to a cardiac patient. I asked the patient about their pain using PQRST and took his vital signs. I gave him nitrates for his chest pain. An EMT came at this point. The patient was still in pain, so I ordered the EMT to set up an IV and administer Morphine. Suddenly on the ECG the rhythm changed from sinus tachycardia to VF. I started compressions and ordered the EMT to attach the pads of the defibb. Once the pads were on, she charged the defibb to 200 J, since its biphasic, and shocked the patient, after ensuring I was clear of the patient.  This lasted two cycles then the patient had a  NSR. I checked for pulse, and it was there. At this point I called the hospital and handed the case over to them and initiated transport. Later on in the session we had another epic OSCE.  My colleagues and I alternated roles between compressing, inserting the igel and ventilating the patient, and setting up an IV to administer Morphine. However, our communication was really bad.

Feelings: At first I felt a little nervous about the OSCE, but once I passed I felt really good. I felt nervous during my scenario since my dad was there but that also slowly subsided and I regained my confidence. Finally, the epic scenario was great and it felt so good to do even better than last week, except for the communication.

Evaluation: The OSCE was a really good experience. The scenario started as a bad experience but once I got through it I realized it was really good. The epic OSCE was a great time. My colleagues and I’s communication with each other was bad but other than that we did really well. Not recognizing the breath sounds was a bit of a setback for me.

Analysis: I shouldn’t have felt nervous during my scenario since I knew what I had to do. Being nervous only limited my abilities.

Conclusion: I could have remained calm and focused to perform the best I can. Also, I could have talked with my team and agreed with them on what each of our roles was going to be. This is to avoid unnecessary chaos and confusion. Also, when auscultating the chest I should take my time to listen to the patient’s breathing to correctly recognize the breath sounds.

Action Plan: I plan to listen to different breath sounds online to be able to recognize  them next time. Also, I plan to remind myself to stay calm and composed no matter what to provide the best possible care. Finally, I will practice my communication skills.

Domain Knowledge:

Aneurysm is a sac formed by the localized dilatation of the wall of an artery, a vein or the heart. Can be fusiform or saccular. 

Risk factors: HT, atherosclerosis, genetic.

Aortic aneurysm presentation depends on site of dissection. Presents with pain to the back, hypotension, pallor, cool, mottling distally, ripping/tearing sensation, impending doom, variable BP. Presentation similar to ischemic cardiac arrest pain.

Management: Do not give fluid (will increase afterload, causing further damage at aneurysm), or make the pt. walk or loosen their belt. 

Pericarditis caused by unknown, bacterial infection, viruses, parasites, post MI, heart surgery, rheumatic fever, rheumatoid arthritis, AIDS. Diagnosis is often recurrent, severe chest pain(sharp, severe, constant), exacerbated by lying down and inspiration, relieved by leaning forward. Also, diffuse ST elevation in all leads. (Pericarditis all around the heart)

Hyperkalemia: Serum K>5.5mEq/l. Increased K causes major changes to ECG.

6.5-7.5 mEq.L: tall peaked Twaves, short QT interval, prolonged PR interval

7.5-8mEq/L: QRS widening and flattening of P wave

10-12 mEq/L: Widened QRS and tall T wave

Hypothermia produces osborn waves when T<32C. Bradycardia and pulseless in severe cases.

LBBB most commonly due to blockage of anterior fascicle of left BB.

Inspiration, palpation,movement, and coughing can produce chest pain.

Takotsubo majority are women who suffer this (cause women are too emotional). Often occurs after bad news. Presents as HF due to impaired LV function. Angiogram shows coronary arteries not blocked so can't be LVF. Normally resolves in up to  months.

Enquiry and Research:

A heart suffering Takotsubo resembles a Japanese pot used to collect an octopus called takotsubo (Sharkey et al., 2011).

Takotsubo presents as an AMI (Golabchi &Sarrafzadegan, 2011).

References

Golabchi, A., & Sarrafzadegan, N. (2011). Takotsubo cardiomyopathy or broken heart syndrome: A review article. Journal of Research in Medical Sciences, 16(3), 340-345. 

Retrieved from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3214344/

Sharkey, S.W., Lesser,J.R.,& Maron, B.J. (2011). Takotsubo (Stress) Cardiomyopathy. Circulation, 124, e460-e462. doi: 10.1161/CIRCULATIONAHA.111.052662

Week 12

Description: This week we performed the IV OSCE, and I passed. After that we practiced approaching a cardiac patient again. I followed the systematic approach and did very well. After that, suddenly, when we were done my teachers changed the rhythm on the mannequin to be a VF and asked us what we will do. Aya started CPR and Asma was attaching the pads of the AED. In that moment, my teacher told me to insert an advanced airway. I quickly ran to the store and got an i-gel. I lubricated it and inserted it in the patient’s airway and started ventilating at a rate of 8-10 breaths/min. Then my teacher told Asma to administer Morphine so she went to prepare the IV set. I took over defibrillating the patient while providing breaths. Aya and I kept alternating, her doing CPR and me on the defibrillator and airway then her on the airway and defibrillator and me on the chest. This scenario kept going for around 15 minutes. The rhythm kept changing from VF to NSR. But when we would check the pulse, there was none. It was PEA. So we would continue CPR. The last rhythm was PEA, and my colleague shocked the patient, putting me, as I was doing compressions, into arrest in the process. This ended the epic scenario.

Feelings: I passed the OSCE so I felt REALLY good! After that I felt confident of my approach to the cardiac patient. In the epic scenario I felt a thrill and was so excited. At first I was confused but that subsided as we went through the scenario. I had so much fun and felt it was the best lab session of the whole semester, in my opinion. However, at the end of the session I felt so tired, but still it felt so good!

Evaluation: This whole session was so good and there was nothing bad about it. I learned so much!

Analysis: After this session, I realized how much I’ve learned this semester, and this made me so happy. It surprised me but it was certainly a great surprise.

Conclusion: The only thing is that I could have communicated with my partner in a better way. This could have helped avoid shocking a PEA, since I knew we had to continue CPR without shocking the patient.

Action Plan: I plan to communicate better with my partner and when placed in such a situation, to act fast and not pause in confusion. Also, I plan to exercise more to increase my stamina, so that I can perform CPR for longer periods without getting tired.

Domain Knowledge:

In neonates congenital heart defect (CHDs) are the most common and there are 35 types. Risk fators include maternal infections (Rubella, Herpes, inta-uterine infection) ,metabolic disorders (diabetes, hypercalcaemia), drugs (alcohol, lithium, warfarin), chromosomal abnormalities, where up to 50% of Down syndrome babies have a CHD! Other risk factors include increased maternal age, prematurity, and family history. 

Patent ductus arteriosus: Aorta and Pulmonary artery connected. Not obvious at birth and if left untreated causes shunting from left to right. Can lead to pulmonary overload and eventual HF.

Atrial septal defect: Interatrial septum open. Causes shunting of blood from left to right side of heart. Mostly asymptomatic. Causes increased pulmonary blood flow but rarely pulmonary HT. Found by routine heart auscultation and repair is carried out to prevent HF, AF and embolic events.

Patent foramen ovale: form of atrial septal defect. Normally closes soon after birth but, abnormally, it stays patent.

Ventricular septal defect: there is an opening between the ventricles. Most common type of CHD. Shunt from left to right and may not be apparent at birth.

Tetralogy of Fallot: Includes 4 things: Pulmonary stenosis, thickened RV wall, ventricular septal defect, and aorta overrides septal defect. Results in right to left shunt and cyanosis. Can be surgically repaired. 

Coarctation of Aorta (COA): narrowing of the aorta mostly around the junction of ductus arteriosus. Depends on timing of closing of ductus arteriosus and location of COA.

Aortic stenosis: Diseased aortic valve. Asymptomatic but can develop exercise intolerance. Depends on severity. Tends to be progressive and can lead to sudden cardiac death, left ventricular hypertrophy and heat failure. 

HF in children presents as: poor feeding, dyspnea, tachypnea, retractive respirations, grunting, nasal flaring, pallor or mottling. Usually discovered after baby goes home.

Sudden death: Can occur at any age secondary to undiagnosed cardiac disease.

Pediatric cardiac diseases are dysrhythmias, Kawasaki disease, systemic HT, childhood obesity, cardiomyopathy, and valvular dysfunction.

Rheumatic fever: Streptococcal infection common in children. If untreated can lead to rheumatic heart disease (RHD). Develops as a sequel to pharyngeal streptococcal infection. Risks include: poor hygiene, overcrowding, underprivileged populations.

In younger adults some diseases include: Obesity related heart disorders, HIV complications, dysrhythmias, and drug use leading to dysrhythmias and cardiomyopathy.

Adult cardiac diseases include: IHD, Prinzmetal angina, ACS, Pericarditis, pericardial effusion, complications from HIV.

Cardiomyopathy is due to ventricular dilatation.  Mostly unknown cause but some known causes include: Ischemic heart disease, diabetes, renal failure, alcohol abuse, drug toxicity, and nutritional  deficiency. 

Hypertrophic Cardiomyopathy/ Hypertrophic Obstructive Cardiomyopathy: thickening of septal wall restricting ventricular outflow. Genetic. Decreased ventricular compliance and exercise intolerance. S&S: SOB, angina, syncope, palpitations, and sudden death. Two types: Hypertensive and restrictive. First one due to HT or valvular stenosis and second one because of rigid, non-compliant myocardium leading to reduced ventricular filling (common symptom RHF).  

Elderly cardiac diseases include CCF, LVF, RVF, intractable angina.

There are some cultural issues that most be dealt with with caution and they involve commencement and stopping resuscitation, agressive or palliative care, and family needs.

Heart Transplant patients have specific complications that result from the body's immune system attacking the transplanted heart. Can be hyperacute, acute orr chronic. Patient is more prone to infections due to immunosuppressants.

Enquiry and Research:

Sudden Cardiac Death is greater in athletes compared with their nonathletic people. This is due to the  strenuous exercise of an athlete that poses an increased risk in undiagnosed cardiac abnormalities. Typically this occurs as a ventricular arrhythmia, due to exerciseinduced catecholamine release acting on an arrythmia inducing substrate (Chandra et al. 2013).

Syncope that occurs during exercise is strongly associated with cardiac syncope. Moreover, if a patient has transient loss of consciousness while lying down this is a sign of the possibility of cardiac syncope. Patients with cardiac syncope eaxperience a rapid reassuring sense of wellbeing on regaining consciousness, due to endogenous sympathetic activity arising in response to the underlying cardiac condition. Auscultation, peripheral edema, raised jugular venous pressure can imply CAD and provide evidence for possible structural heart disease. Cardiac syncope with the presence of structural heart disease are both associated with increased risks of future sudden death (Anderson & O'Callaghan, 2012).

References

Anderson, J., & O'Callaghan, P. (2012). Cardiac syncope. Epilepsia, 53(7), 34-41. doi: 10.1111/j.1528-1167.2012.03713.x

Chandra, N., Bastiaenen, R., Papadakis, M., & Sharma, S. (2013). Sudden cardiac death in young athletes: Practical challenges and diagnostic dilemmas. Journal of the American College of Cardiology, 61(10), 1027-1040. doi: 10.1016/j.jacc.2012.08.1032

Week 11

Reflection:

Using the Gibb’s Reflective Model I will reflect on the tenth Lab session we had for this semester. It took place on the 11th of  November.

Description: This week in the morning when we arrived we practiced calculating a drip rate and preparing an IV set, priming it and actually counting the drip rate in the chamber. Later on in the day we practiced this skill again and added to it administering drugs. We practiced administrating Morphine in the Y port and the 3 way tap. Later on we worked through the defibrillation workbook. After that we discussed defibrillation, shockable rhythms, identifying them and the steps to performing safe and effective defibrillation. We also talked about the benefit of pads compared to paddles. Proceeding that we looked at the OSCE marking sheet for defibrillation and went through it step by step with our teacher.

In the second session we practiced setting up an IV and administrating drugs again. After that we looked through the OSCE sheet for IV preparation and drug administration. Following that our teachers assessed us on this skill against the OSCE sheet, in preparation for our OSCE next week. Proceeding, we practiced out approach to the cardiac patient. I was given a 50 yr old female with chest pain and a history of angina and HT. I followed the systematic approach and asked questions pertaining to history taking using PQRST  and conducted a VSS. The VSS included an ECG, which I asked for a 12-lead when the 3-lead showed a normal rhythm. Also, I took the SpO₂ , BP, and HR. The patient was hypertensive but everything else was normal. After that I decided to transport the patient due to increasing pain. On the way to the hospital I continued taking the patient’s history using SAMPLE.

Feelings: I felt really excited in these two lab sessions. They were so much fun. I felt confident with my IV setting up and administering Morphine and in the second session, I felt even more confident and excited. Learning about defibrillation and working through the workbook for it was really interesting for me. I felt really intrigued by this skill and felt relaxed when we were going through the OSCE sheet, since it was very simple. In the scenario I felt confident, put together, and I felt really good at the end of it, since I did much better than the week before.

Evaluation: The whole session was a good experience that helped restore my confidence and reminded me of why I love this profession.

Analysis: After this week I realized that I must mess up in order to do better the next time. It has been a real learning experience for me.

Conclusion: The only thing I would have done differently is provide analgesia to the patient while transporting her.

Action Plan: Review the IV and defibrillation OSCE sheets. Also, I plan on researching Morphine and learning more about it, such as its dose, contraindications and effects.

Picture 1: Administering Morphine in the Y port

Domain Knowledge:

Heart failure, also known as chronic heart failure, is when the heart is unable to pump adequately to meet the needs of the body. S&S: SOB, paroxysmal nocturnal dyspnea, leg swelling, and exercise intolerance. It is caused by MI, HT, Valvualr disease, ischemic heart disease, and cardiomyopathy. In the failing heart Starling's law does not apply to the heart. If preload increases too far the failing heart can not maintain output and the ventricles will fail.

Ejection fraction= SV/EDV x100. Where SV= EDV-ESV

Normally around 60%, in heart failure it drops below 40%.

Concepts for treating HF includes reducing the preload and afterload.

Treatment includes: Medication, such as vasodilators and diuretics, pacemaker, ventricular assist device, and heart transplant.

Increased venous return -> increased preload and afterload -> Acute LVF (pulmonary hydrostatic pressure overcomes plasma oncotic pressure.)

Results in increased Pulmonary pressures. If MAP is over 25mmHg, hydrostatic pressure starts to overcome oncotic pressure. This causes fluids to shift from pulmonary capillaries to the interstitium and then into alveoli causing alveolar flood-> Acute pulmonary oedema (APO)

Paramedics can have a significant effect on APO. Nocturnal dyspnea due to increased venous return, non-compliance with diuretics or anti-hypertensives, and increased fluid intake at night. Upon auscultation, paramedics can hear wheezes due to the fluid in the interstitium, fine crackles (fluid in alveoli), Alveoli can collapse due to loss of surfactant, this can be heard as fine crackles upon inspiration.

Prehospital treatment includes: Oxygen, GTN to decrease afterload, Morphine, continuous positive airway pressure ( CPAP), Frusemide. Patient with LVF or APO should never be allowed to walk, exertion must be a minimum.

CPAP maintains intra-thoracic pressure to keep airways open and maintain gas exchange. Patient must spontaneously ventilate. If have respiratory failure -> intubation.

Right ventricular failure (RVF) results from chronic LVF, or can be due to RV infarct, pulmonary valvulopathy, or cardiomyopathy. It causes peripheral edema, hepatosplenomegaly, and jugular venous distension due to increased preload. 

Cardiogenic shock is persistant hypotension and tissue hypoperfusion caused by cardiac dysfunction in the presence of adequate intravascular volume and left ventricular filling pressure. Has a high mortality rate,Caused by AMI, cardiomyopathy, spesis, myocarditis, dysrhythmmias leading to impaired diastolic filling, metabolic abnormalities, papillary muscle rupture, PE, Cardiac tamponade, and valvular disorder.  Can also be caused by inferior and anterior AMI. If during an ECG the rhythm looks normal but the patient doesn't -> perform 12 lead ECG.

For cardiogenic shock treat the cause if possible.

Enquiry and Research: 

Systolic dysfunction is the most common cause of heart disease in Western societies. Although both sysolic and diastolic CHF coexist, it is very important to distinguish between them when it come to treatment. The best treatment, however, is patients learning to manage their CHF . This is done by restricting fluid intake, adhering to a complex medication regimen, maintaining a low sodium diet and engaging in physical activity. Also, evidence suggests the benefits of using biventricular pacing in HF to resynchronise cardiac contraction and improve ventricular performance (Massey & Williams, 2011).

I read further on the different causes of HF. The following are the bits i found helpful:

Picture 2: Mechanisms of atherosclerosis and persistent HT on HF. Adopted from ( Marieb & Hoehn, 2014).

Picture 3: Mechanisms of multiple MIs and dilated cardiomyopathy on HF. Also, results of LHF. Adopted from ( Marieb & Hoehn, 2014).

Picture 4: Results of RHF. Adopted from (Marieb & Hoehn, 2014).

It is uncommon for patients with HF to have a normal ECG. Therefore, if the ECG is normal an alternative diagnosis must be considered.

Also, mentioned earlier GTN and furosemide are used to treat HF. However, prehospital trials comparing administration of furosemide vs. GTN and found that GTN was better. Therefore, furosemide must only be given after nitrates (JRCALC, 2013).

Picture 5: Algorithim for HF. Adopted from (JRCLAC, 2013). 

Morphine presents as an ampule with 10mg/ ml. It is a strong opioid analgesic. It depresses  respiration and induces hypotension. Given via IV route and needs 2-3 minutes to start acting. Reaches its peak between 10-20 minutes. Morphine should be diluted with 0.9% normal saline to make a concentration of 10mg/10ml. Start with minimal dose and increase by 2 mg every 3 minutes if pain doesn't go. Maximum dose is 20 mg! (JRCALC, 2013).

Picture 6: C/I of Morphine. Adopted from (JRCALC, 2013).

 References

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

Marieb, E.N, & Hoehn, K.N. (2014). The cardiovascular system: The heart. In E.N. Marieb & K.N. Hoehn (Eds.), Human anatomy and physiology (713-741). Essex, England: Pearson Education.

Massey, S.L., & Williams, B. (2011). Cardiovascular emergencies. In K. Curtis & C. Ramsden, Emergency and trauma care for nurses and paramedics (489-533).Chatswood, NSW: Mosby

Week 10

Reflection:

Using the Gibb’s Reflective Model I will reflect on the ninth Lab session we had for this semester. It took place on the 4th and 5th of November.

Description: This week we solved the IV therapy workbook and spent the first hour learning about how to perform an aseptic technique when handling needles and equipment, how to insert an IV cannula, calculate the drip rate, set up an IV set, connect it to an extension, connect the IV line to a IV bag and prime the IV line. For this part of the session I understood where everything went and how it all worked. I was also able to correctly calculate the drip rate. Also, my teacher showed me how to improvise by hanging the IV fluid on a spine board to free my hands. In the second hour, we practiced the approach to a cardiac patient. I went first and my patient was diaphoretic and had difficulty breathing. I had good communication with the patient, remembered to do an ECG this time, gathered the history appropriately, and performed the VSS. However, after I found out the patient had dyspnea it took me a few minutes before I auscultated her chest. Moreover, I saw her SpO₂ was 89% so I decided to give her oxygen.  When I provided her with oxygen, I used a nebulizer mask instead of a non-rebreather mask. This was a terrible mistake. However, my teacher notified me of my mistake and I fixed it. A while after I put the  non-rebreather mask on the pt., her SpO₂ went up to 96% and I instantly, without thinking, removed the mask, only to put it back on a few minutes later when the SpO₂ dropped. After that I discovered the patient was diabetic, however, it slipped my mind to take a BGL measurement and also that diabetic pts. usually present with no chest pain during an MI. The patient’s ECG rhythm was sinus tachycardia, and I said I would perform a 12-lead ECG to check for a possible infarction that wasn’t visible on a 3-lead.

 In the next session, we further practiced IV cannulation and setting up an IV line. After that we performed another cardiac patient scenario. My patient presented with severe chest pain and difficulty breathing. He was tahcycardiac and hypertensive and his ECG rhythm was sinus tachycardia. I took all the history using PQRST and SAMPLE and performed a thorough VSS. This time I used a non-rebreather mask to deliver oxygen to the pt. As the scenario progressed the pt.’s rhythm suddenly became an ST elevation. I decided to provide morphine, nitrates, aspirin, and continue oxygen administration. My teacher later remarked I could have also prepared double cannulas to prepare for any possible upcoming emergency.

Feelings: At the beginning of the first session I felt really excited to learn about the preparation process of IV equipment. Later on, right before I started the scenario, I felt confident, but that changed really quickly. As I progressed through the scenario I made multiple mistakes and I didn’t feel very confident and felt lost and confused. My systematic approach was all jumbled up in my head and I was struggling to fully understand the scenario. By the end of that session I felt upset at myself for messing up so bad.

In the second session, for the IV practice I felt at ease and capable, since I understood everything the day before. After that, when we were practicing a cardiac patient scenario, I felt nervous at the start. However, I stuck to the systematic approach this time and managed the scenario well. This made me feel so good and when my teacher said I did very well, I felt much more confident. 

Evaluation: Learning about IV preparation was a really good experience, since I understood everything involved in the process. Also, it was great to be able to practice this skill individually. This made me more aware of every step of the process, which helped me understand everything. I would say the scenario in the first session was a bad experience, however, without it I don’t think I would have been able to do as well the next session. It was good to make all those mistakes because it was like a wakeup call for me to step up my game. This made my experience in the second session so much better. Also, being able to know my mistakes the first time and fixing them in the next session was a really good learning experience for me.

Analysis: My mistakes in the first scenario were due to a lack of organization of my thoughts. I didn’t follow a systematic and logical approach and that lead to me missing out crucial steps. For example,   BGL measurement for the diabetic patient is something I know. However, I didn’t preplan my approach or think logically about the scenario, and that lead to me missing that important assessment. Also, now I realize that if I start a scenario without a set plan I am bound to forget things and end up confused. In the second session I revised my approach and that was the key to me performing much better.

Conclusion: I could have been more focused and thoughtful of what was unfolding throughout the scenario. Also, I should have revised the steps for approaching the cardiac patient beforehand. This could have lead me to assess the patient appropriately and not forget anything.

Action Plan: My plan is to revise the OSCE marking sheet for approaching the cardiac patient. This is in order for me to be able to have a pitch perfect and systematic approach, and to stop me from forgetting anything. Moreover, I will look through the OSCE sheet for IV preparation and practice drug calculations. That is to be prepared for the next session, in which we will be preparing an IV set and calculating and counting the drip rate.

Picture 1: Calculation of the drip rate

Picture 2: IV cannula inserted and IV set primed

Picture 3: IV fluid hung on a spine board to improvise

Picture 4: IV chamber with set drip rate

Domain Knowledge:

This week we took about pacemakers. Sick sinus syndrome is the general term for a group of dysrhythmmias caused by the malfunction of the sinus node. Most commonly caused by ischemic heart disease. In this case the patient must be paced using a pacemaker. A pacemaker can be external, tansvenous or implantable. On an ECG its very obvious. 

Picture 5: ECG with a pacemaker

Transvenous pacing is done in the ED in hospital. It when an electrode is advanced under fluoroscopy to place the electrode. This is temporary. For implantable pacemakers there are two. fixed rate and demand. Demand is usually used and it senses the patient's intrinsic rate, specifically the QRS complex, and will only fire when the intrinsic rate falls below a set rate. Fixed rate fires at a constant rate regardless of the patient's intrinsic rate. 

Pacemakers can be atrial, ventricular, or for both (dual chamber). A patient is usually given Aspirin after this to avoid blood from coagulating on the wires of the pacemaker. Pacemakers can also sense the RR and blood pH.

Problems faced by a pacemaker are failure to sense, capture, and pace. Failure to sense in from the pacemaker's failure to sense the heart's intrinsic electrical activity. It generates a pacing spike at inappropriate times. This is very dangerous and could lead to the RonT phenomenon. Failure to capture is when the paced stimulus does not result in myocardial depolarization. The pacemaker spikes are not followed by a P wave or QRS complex. Most likely cause is that the output current of the pacemaker is too low. Failure to sense and capture can occur in the same patient. Failure to pace means the pacemaker is doing nothing. If a patient with a ventricular pacemaker has a STEMI, they cannot be diagnosed from an ECG, they are diagnosed by their history and inhospital ultrasound.

Pacemakers can be placed in both ventricles (biventricular pacing) and this is called cardiac resynchronisation therapy (CRT).

Some indications for implanting a pacemaker in a patient are:

• The patient has had a past episode of VF or VT arrest
• had at least one episode of VT
• had a previous heart attack and an increased risk for sudden cardiac arrest or death
• hypertrophic cardiomyopathy

Implantable defibrillators have an energy level of 35-40J. Low compared with surface defibb, cause surface defibb must go through all layers of the thorax before reaching the heart. Thus needing a high level of energy. But the implantable one is directly on the heart. It's leads are biphasic and for cardioversion the energy can be as low as 2J. 

Enquiry and Research: 

Pacemakers consist of a controller pack that contains the battery and programmable hardware and wire electrodes that are attached to the heart chambers that need to be stimulated (Wesley,2011).

Pacemakers have two functions: to sense the atrial and/or ventricular electrical activity and the second is to pace, during which the electrode generates and electrical discharge to depolarize the myocardium. The timing cycle consists of a lower rate limit (LR) and a ventricular refractory period. If an intrinsic QRS complex occurs the LR time is started from that point. If there is no QRS and the LR is reached the pacemaker will spike.

Picture 6: Table of the pacemaker codes. Adopted from (Wesley,2011)

Letters 1,2,3 are the most commonly used letters and provide sufficient information about how the pacemaker functions, helping in the interpretation of the associated ECG rhythm.

Implantable cardioverter defibrillator therapy (ICD) involves the internal placement of a device capable of delivering electrical shocks to the heart to terminate life threatening rhythms, such as VT and VF. Like the pacemaker except instead of a simple electrode in the rt ventricle, there is a special electrode touching more surface area of the endocardium. This electrode delivers the life-saving shock to the heart in the event of lethal ventricular dysrhythmmias. It can deliver anitachycardia pacing and cardioversion shocks for VT and defibrillation shocks for VF (Wesley, 2011).

Picture 7: Reading from (Wesley, 2011).

Picture 8: Readings from (Wesley, 2011)

When ICDs are delivering shocks inappropriately, they can be disabled using a ring magnet. This magnet can temporarily disable the shock capability of an ICD. However, the magnet does not disable the pacing capability for treating bradycardia.The ECG rhythm must be monitored at all times  when the ICD is disabled. These magnets are usually supplied by the manufacturers (JRCALC, 2013).

A really good illustration of the pacemaker in the heart is found on the following link (AHA, 2015). The one in the illustration is a ventricular pacemaker. The link is: http://watchlearnlive.heart.org/CVML_Player.php?moduleSelect=pacmkr

This illustration helped me visualize the effect of the pacemaker on the heart.

References

American Heart Association. (2015). Pacemaker [Video illustration]. USA: Watch, Learn, and Live Interactive Cardiovascular Library.
Joint Royal Colleges Ambulance Liaison Committee. (2013). UK ambulance services: Clinical practice guidelines 2013. Bridgwater, England: Class Professional Publishing.

Wesley, K. (2011). Huszar's basic dysrythmias and acute coronary syndromes: Interpretation and management (4th ed.). St Louis, MO: Elsevier.

Week 9

Reflection

Using the Gibb’s Reflective Model I will reflect on the eighth Lab session we had for this semester. It took place on the 28th of September.

Description: In this week’s lab sessions, we further practiced our approach to a cardiac patient, in order to perfect it. First, we revised the OPQRST acronym and what it means. After that I was given a scenario of a 50 year old female with chest pain, and this time I used the PCR and asked all the required questions. This time I used OPQRST instead of DOLOR+S in my pain assessment. I remembered everything except performing an ECG, but then my teacher reminded me. Later I had a second chance at repeating the scenario, but this time my peers were assessing me. This time around I remembered everything except asking about the duration, and I was confused as to why I should ask about duration of pain if I already asked about onset. However, I asked my teacher later and he explained how the pain levels change and I need to know the duration of each level of pain. In the next lab, my peers and I repeated the scenario to further practice, however, we didn’t have any equipment. On that day we learned about the importance of informing our teachers of our plans, in order for us to be able to book all the equipment we need.

Feelings: This time around I felt much more confident in my approach and I saw the improvement, from not knowing what to ask, to this week, having a systematic approach. Moreover, I felt at ease and more confident when my peers were the ones assessing me, and I didn’t forget anything then, compared to when my teacher was the assessor. However, the next day, I felt a bit disappointed when I found out we couldn’t use the equipment and the whole day was going to go for nothing.

Evaluation: It was very good that we got to revise the OPQRST before we started. This helped boost my memory and understand the acronym better. Also, it was a good experience being able to remember and perform almost everything correctly. Using the PCR helped me greatly to recall everything about the patient’s information. Furthermore, It was really nice to have my peers assess me, since this disposed of any pressure I felt and helped me perform better. However, I felt dissatisfied when I discovered I had forgotten to perform an ECG and, also, when I couldn’t practice with the equipment.

Analysis: During the scenario, when I was faced with a patient complaining of chest pain, I should have had doing an ECG at the top of my mind. Moreover, I should have considered that the student’s younger than me have a lab that day and would need the equipment. Therefore, it was vital to tell my teachers in order for them to know we were coming, to allocate some equipment for us.

Conclusion: In the end, I learned that good and thorough patient assessment and history taking can be the difference between life and death. Moreover, using the PCR is vital to record all the patient’s details in case of forgetfulness on my part. Also, an ECG should always be done on any suspected cardiac patient. Moreover, peer teaching, as Boud (2013) mentions, can help students to learn effectively. Furthermore, it is important to always keep my teachers in the loop, and informing them of any plans my peers and I have. That is in order for our plans to actually work.

Action Plan: My plan is to keep practicing my approach to the cardiac patient until it is pitch perfect, to always use a PCR, and remember the essential need for an ECG examination for such a patient. Also, I will use some of my free time to practice with my peers and ask them to assess me. Lastly, I will inform my teachers of any plans I have for practicing, and book any equipment I’ll need for that.

Picture 1: My colleagues evaluation of my performance during my scenario

Reference

Boud, D. (2013). Introduction: making the move to peer learning. In D. Boud, R. Cohen, & J. Sampson (Eds.), Peer learning in higher education (pp. 1-20). Retrieved from http://www.amazon.com/Peer-Learning-Higher-Education-David/dp/0749436123

Domain Knowledge:

This week's lecture we further discussed ACS. First, we discussed the clotting process that occurs when a plaque rupture. 

Picture 2: Flowchart of the clotting process

This process happens through a cascade of clotting factors from an intrinsic and extrinsic pathway. This cascade ends with the formation of prothrombin activator. This is an enzyme that converts prothrombin into thrombin. Thrombin then converts fibrinogen to fibrin which forms fibrin strands that provide an insoluble mesh that holds the platelets.

When a STEMI occurs there are various interventions to manage it. They include:

• Antiplatelet agents
• Anticoagulant therapy
• Glycoprotein IIb/IIIa inhibitors
• Reperfusion therapy. Could be PCI or fibrinolytic therapy
• And the best treatment, percutaneous coronary intervention (PCI)

Picture 3: Flowchart of different treatments of ACS.

Early recognition, rapid transport and treatment are vital!!

PCI improves short term and long term outcomes in patients with STEMI presenting within 12 hours compared to fibrinolytic therapy. However, the benefit only occurs if the difference between time to fibrinolytic therapy and time to balloon is less than 1 hour!

If PCI is not available or is delayed, reperfusion with fibrinolytic therapy should occur.

For best outcomes fibrinolytic therapy is administered within 12 hours or less after the onset of symptoms. The most commonly used is tissue plasminogen activator, such as tenectaplase. The efficiency of fibrinolytic drugs depends on the age of the clot.

Contraindications for fibrinolytic therapy are cerebral event within 6 months, major trauma including surgery within 1 month, bleeding peptic ulcer within 2 months, uncontrolled HT, and non-compressible vascular puncture.

Serum Markers have a high sensitivity to AMI and enable the diagnosis of AMI. There are 3 main markers: Creatine Kinase, CK MB, and Troponin.

Creatine Kinase	·          Enzyme specific to brain, myocardium, skeletal muscle ·          Diffuses from damaged cells into blood after irreversible injury ·          CK increases caused by AMI, UA, shock, cardiac surgery, ventricular arrhythmias, CPR and IM injection ·          Elevate within 4-8 hrs after coronary occlusion, peaks at 12-24 hrs and returns to normal within 3-4 days
CK MB	·          Specifically in cardiac muscle cells ·          Not accurate specificity for diagnosis of AMI. Released also in liver disease, exertion, cocaine use, renal failure ·          Detected 4-6 hrs after occlusion, peaks at 12-24 hrs but cleared within 48 hrs.
Troponin	·          Troponin I and T both in cardiac myocytes, Troponin I cardiac specific ·          Levels rise with minimal necrosis ·          Become elevated after 6 hrs, peaks at 12 hrs and remains elevated for 7-10 days ·          Any range above 0.1µg/ml could be indicative of myocardial injury or infarction

Table 1: Common Serum Markers and their characteristics

Post AMI management includes Beta blockers, ACE inhibition, antiplatelet agents, anticoagulation, and statins. Also there are complications associated with AMI, as can be guessed. These include arrhythmias, pulmonary edema, severe mitral regurgitation, ventricular septal rupture, ventricular aneurysm , ventricular thrombus, and pericarditis. 15-40% of MIs will have a degree of CCF and 5-8% will have cardiogenic shock. Cardiogenic shock implies 40% myocardium loss and has a mortality as high as 80% which can only be altered by PCI or CABGs. Some mechanical complications include ventricular wall rupture, septal rupture, and papillary muscle rupture. Pericarditis occurs in 10-20% of all AMIs and is more common in STEMIs. It is often confused with infarct extension or post MI angina. LV thrombus requires warfarinization after initial care and can cause arterial embolus and PE.

Enquiry and Research: 

I did some further readings and the following are my notes from them.

Picture 4: The pathophysiologic continuum from atherosclerosis till MI.

Picture 5: Atherosclerosis and the results of stable and unstable plaques. Adopted from (Brashers, 2006, chap.30)

Picture 6: Flowchart of summary of processes leading to ACS. Adopted from (Brashers, 2006, chap.30)

Cardiac cells can withstand ischemic conditions for 20 minutes. Recurrent myocardial ischemia can result in myocyte adaptation to oxygen deprivation and preservation of myocardium. This is called ischemic preconditioning (Brashers, 2006, chap.30).

Coronary angioplasty is the most common PCI. Balloon angioplasty increases the size of the lumen through endothelial denudation. The greater the increase in lumen size, the lower the risk of re-stenosis. However, aggressive balloon inflation can lead to excessive dissection, platelet deposition, thrombus formation and plaque hemorrhage. Pericarditis is more common in patients with transmural AMI(Hollander & Diercks, 2011, chap. 53).

In the interpretation of Troponin levels, a limit as low as 0.01ng/mL can be set on high-sensitivity cTn assays. This makes it possible to identify patients with ACS earlier, enabling earlier coronary intervention.  The cTn results, however, must be interpreted in the context of the clinical history, ECG findings to establish the correct diagnosis. This is because elevated cTn may be detected in conditions other than ACS, including heart failure, renal failure, tachyarrhythmias, PE, and even after strenuous exercise in healthy individuals (Mahajan & Jarolim, 2011). 

I didn’t understand what transmural and nontransmural MIs meant, therefore I conducted a search to find out. I found an article that explained the difference. Transmural MI is characterized by ischemic necrosis of the total thickness of the muscle segment affected, from the endocardium through to the epicardium. On the other hand, nontransmural MI is when the area of the necrosis is limited to the endocardium and sometimes it extends to the myocardium (Bolooki & Askari, 2010).

Finally, in the AHA 2015 ECC and CPR guidelines it is said that prehospital providers should transport a patient with STEMI directly to a PCI center even with the availability of fibrinolysis. This protects the patient from the incidence of intracranial hemorrhage. Also, when fibrinolytic therapy is administered to a STEMI patient, it’s better to transport all postfibrinolysis patients for early angiography, in first 3-6 hours and maximum 24 hours. Rather than transporting them when they REQUIRE ischemia-guided angiography (AHA, 2015).

References:

American Heart Association. (2015). Highlights of the 2015 American Heart Association Guidelines update for CPR and ECC. Retrieved from https://eccguidelines.heart.org/wp-content/uploads/2015/10/2015-AHA-Guidelines-Highlights-English.pdf

Bolooki, H.M., & Askari, A. (2010). Acute myocardial infarction. Retrieved from http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/cardiology/acute-myocardial-infarction/#top

 Brashers, V.L. (2006). Alterations of cardiovascular function. In K.L. McCance & S.E. Huether  (Eds.), Pathophysiology: The biologic basis for disease in adults and children (pp.1081-1146). St. Louis, MO: Mosby.

Hollander, J.E., & Diercks, D.B. (2011). Acute coronary syndromes: Acute myocardial infarction and unstable angina. In J.E. Tintinalli (Ed.), Tintinalli's emergency medicine: A comprehensive study guide (pp.367-385). New York, NY: McGraw Hill

Mahajan, V.S., & Jarolim, P. (2011). How to interpret elevated cardiac troponin levels. Circulation, 124, 2350-2354. doi: 10.1161/CIRCULATIONAHA.111.023697