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