Week 7

Reflection

Using the Gibb’s Reflective I will reflect on the sixth Lab session we had for this semester. It took place on the 14th of October.

Description: I was given a scenario of a young cardiac patient. Demonstrating a correct approach and logical sequence of history taking was required from me. I had two attempts because the first time I did not follow the right sequence, however, in my second try I was able to demonstrate the correct sequence. The sequence included conducting the primary survey, DRABCH, through asking the patient her name and age. Following that, I attached the SpO₂ probe and BP cuff to start my VSS and started inquiring about the patient’s condition and medical history using DOLOR+S and AMPLE.

Feelings: In my first attempt, I asked a question not included in the clinical approach, and that made me get confused. However, in my second try I focused on following the right order of assessment, in order to avoid forgetting anything.

Evaluation: It was good for me to be able to repeat my scenario in order to rectify my mistakes and start the scenario in the right way, to avoid making mistakes due to confusion and lack of order. I did a good job in my primary survey, however, when it came to the VSS I did not attach the patient to an ECG, even though I was aware she was a cardiac patient. Moreover, I did not document the information my patient provided in the secondary survey and by the time the scenario was over I forgot important information. For example, I forgot the other signs and symptoms, nausea and dizziness, which are crucial signs and symptoms for the diagnosis of cardiac diseases, such as SVT.

Analysis: I could have been more thorough in the PCI. For example, when I asked about the patient’s medications I did not ask her how long ago she took it. Also, I did not ask for the time of last oral intake. This information would have been useful if acquired.

Conclusion: It is very important to conduct a thorough VSS and PCI as soon as possible, because the patient’s condition can deteriorate at any moment. Also, not obtaining all the information relevant to the case can mislead you. Moreover, it is crucial to follow a systematic approach and document all the acquired information to avoid forgetting anything.

Action Plan: Next time I will follow the clinical approach sequence thoroughly and bring the PCR with me to document all the information I obtain regarding the patient. This is in order for me not to miss anything. Furthermore, I will perform an ECG examination as soon as I find out my patient is of cardiac nature.

Picture 1: The jumpbag and iSimulate that were used by me during the scenario

Domain Knowledge:

CVDs include coronary heart disease, cerebrovascular disease, peripheral arterial disease, rheumatic heart disease, deep vein thrombosis, and pulmonary embolism. 
Nonmodifiable risk factors are age, sex, family history, and ethnicity. Where age is the most powerful risk factor that doubles the risk of CVD for every decade after the age of 55. Males have a higher risk of CVD and the risk increases if a first degree blood relative had a CHD or stroke. The risk is commonly high in Indians and Sri Lankans.
Some modifiable risk factors include behavioural factors, tobacco smoking, insufficient physical activity, dietary behaviour, excessive alcohol consumption, HT, high blood cholesterol, obesity and depression. 
ACS refers to a range of symptoms that are compatible with myocardial ischemia. ACS share a common pathophysiological pathway of coronary plaque disruption with superimposed thrombus formation, ranging from superficial adherent thrombi interrupting coronary blood flow to total occlusion that compromizes the myocardial perfusion, leading to ischemic necrosis and eventually to AMI. Three diseases fall under ACS and they are : STEMI, n-STEMI, and UA.
CAD: The presence of atherosclerotic changes in coronary arteries' walls and the potential formation of a thrombosis due to plaque rupture leading to disrupted blood flow to the myocardium.
The endothelium is a mono-layered inner lining of the entire vascular system. It consists of simple squamous endothelial cells. It is the key element to atheroma formation. The endothelium has a nonthrombogenic surface containing a potent vasodilator, inhibitor of platelet aggregation, and is covered in heparin sulphate. It also secretes endothelium-derived relaxing factor, which is a form of nitric oxide. This maintains the balance between vasodilation and vasoconstriction in homeostasis. The endothelium also secretes fibrinolytic agents and cytokines and adhesion molecules, as well as vasoconstrictors. The endothelium regulates the vascular tone, platelet adhseion, monocyte adhesion, inflammation, thrombus generation, lipid metabolism, cellular growth and vascular remodeling. Just recently the focus of atheroma formation has become about the malfunction of the endothelium, which plays an essential role in preventing atheroma from forming.

Picture 2: Atheroma formation flow chart

Picture 3: Plague progression flow chart

Picture 4: Plaque rupture flow chart of events

ST depression: Myocardial ischemia

ST elevation: Myocardial injury

Deep Q waves: Myocadial infarction(death)

When AMI occurs there are 30 minutes until irreversible ischemia occurs. The ischemic area is surrounded by stunned myocardium with reversible ischemia. This causes hypokinesis, and endocardium dies first, followed by the myocardium. During this time anaerobic metabolism is initiated. This produces 5% of the required energy, however, this is critical for stunned myocardium to live. Glycogenolysis occurs for a few minutes after creatinine phosphate and ATP are burnt. Anaerobic metabolism lasts for 40-60 minutes.

Glycolysis causes the Na-K pump to fail, Na-Ca pump to be activated. Both these effects result in cell edema, membrane leak, contractile inhibition, enhanced autonaticity, depolarization, and conduction disturbance. Contraction failure occurs seconds after occlusion with the size of the MI is the most important determinant of pump failure.Diastolic failure occurs simultaneously and worsens relaxation through acidosis, which desentisizes contractile elements. Commonly decreased LV compliance and contractility activate sympathetic nervous system and increase SVR to maintain MAP. If the contractility is severely impaired, the compensation fails. PVR and SVR increase and myocardial O2 consumption increases the worsening ischemia. This process is a cycle and it will lead to heart failure and shock.

Exertional angina is episodic, lasts less than 10 mins, provoked by exertion and is relieved by rest or nitrates. The difference between exertional angina, or stable, and unstable angina is that UA comes from no exertion, suddenly, it is easily provoked and is not relieved by rest or nitrates.

Patients with nSTEMI and UA are almost indistinguishable, that is because they have the same pathogenesis. They are both caused by non-occlusive thrombi which reduce myocardial perfusion. The cardiac pain is believed to be due to microembolization and components of disrupted plaques.

STEMI, on the other hand, is when the thrombus is completely occlusive. This can lead to myocardial necrosis. On an ECG it presents as ST elevation of 1mm or more, in 2 or more leads.

MI diagnosis is based on:

1. history
2. serial ECGs
3. blood enzymes

Patient's will describe the presence of pain, discomfort, tightness, fullness, squeezing, burning pain. It is usually described as severe. The symptoms associated with MI include: diaphoresis, nausea, vomitting, SOB, palpiatations, arm pain, and radiation to the back. The patient will appear sick, normally they will be seated due to dyspnea, and they will be exhausted and panicking. If they are pallor, grey in color, diaphoretic and clammy they are going through a more extensive myocardial injury.

Reproducible chest wall tenderness is usually due to pericardial irritation, however, it could happen during an AMI. This tenderness should not exclude MI in the diagnosis. Also, sometimes AMI will present with pain that is usually considered pleuritic, which is sharp upon movement and inspiration. Anginal symptoms are not severe and are usually noted retrospectively. Sinus bradycardia(50-60 bpm) is common in the first few hours especially in inferior MI. Sinus tachycardia >12-24 hours is predictive of very high mortality. This is when the heart is trying to compensate and once that fails, the heart fails. On average BP is normal but either extreme suggests a worse diagnosis. Bilateral BPs is helpful in the DDx of dissecting thoracic aorta. Respiratory rate is usually normal but respiratory failure occurs very soon after the onset of symptoms. 

ECGs are the most useful tool in determining STEMI in the prehospital setting. Serial ECGs are usually done for higher accuracy. Some patients present with other signs and symptoms of AMI and no chest pain, such as in diabetic patients.

ECG changes in MI are as follows:

1. Normal ECG
2. Hyperacute T waves, increased T wave amplitude and width (0-30 mins)
3. Marked ST elevation with hyperacute T wave changes (0-6 hrs)
4. Marked ST elevation with T wave inversion (6-12 hrs)
5. Pathologic Q waves, less ST elevation, terminal T wave inversion (12-24 hrs)
6. Pathologic Q waves, T wave inversion (>24 hrs)
7. Pathologic Q waves, upright T waves (months to years)

The signs of nSTEMI and UA are convex downward ST segment depression, symmetrical T wave inversion, or a combination of the two.

On physically assessing an ACS patient, the paramedic will find: hypotension/hypertension, which predict poor outcome, diaphoresis, tachypnea, peripheral edema and a 12 lead ECG must be done.

For the treatment of ACS Nitrates are used to relieve pain and it causes vasodilation. It is indicated in large anterior MI, failure, post infarct angina and HT with MI. It should not be used in inferior MI until rt ventricular infarct is excluded. This is because nitrates will cause vasodilation, decreasing the preload. However, the heart needs as much oxygen as possible, and decreasing preload decreases afterload, decreasing the oxygen supply to the mycordium. Aspirin can be given as a 300mg dose. In the ISIS 2 Trial, it was demonstrated that aspirin lead to 23% reduction in mortality in MI. O2 can lessen the level of ST elevation and is useful in the first 2-3 hours of AMI. However, there is some conflicting evidence about this. For pain relief, Morphine can be used, since it decreases the sympathetic nervous system stimulation, decreasing the myocardial demand.

AMI management can be put in a acronym, MONA. This stands for Morphine, Oxygen, Nitrates, and Aspirin. Bilateral IV access is useful in this case.

The main goals of treatment are to reduce amount of myocardial necrosis, preserving LV function and preventing heart failure. Also, to treat acute, life-threatening complications of ACS, such as VF, pulseless VT, symptomatic bradycardia and unstable tachycardia. Quick transport to an appropriate hospital is crucial! Patients with confirmed ACS must be transported directly to a cath lab.

Enquiry and Research:

To really visualize the process of atherosclerosis, I took it onto myself to search for videos that can help me with that. I found:

Two videos by Khan Academy, which provide a summary of the anatomy of blood vessels and a detailed explanation of the causes and the process of atherosclerosis:

1.     https://www.khanacademy.org/science/health-and-medicine/circulatory-system-diseases/blood-vessel-diseases/v/atherosclerosis-part-1

2.       https://www.khanacademy.org/science/health-and-medicine/circulatory-system-diseases/blood-vessel-diseases/v/atherosclerosis-part-2

I further searched for an illustrative video of how atherosclerosis causes a heart attack and found another video, by Khan Academy, which briefly discusses the vessels entering and leaving the heart as well as the coronary circulation. After that it discusses atherosclerosis and its effect on the coronary circulation and the myocardium. It also talks about ischemia and CHD and subsequently heart failure, angina, plaque rupture, clot formation which leads to infarction of the myocardium. Moreover, it differentiates between myocardial infarction(MI) and cardiac arrest, where MI is when some muscle tissue dies. This can lead to cardiac arrest, which is the dying and stopping of the heart. This leads to the death of the person. The video can be found at https://www.youtube.com/watch?v=vYnreB1duro

I found another two videos that illustrate atherosclerosis and acute coronary syndrome in a concise, simple and effective manner. I found these videos very helpful. These are their links

1.      http://www.nucleuscatalog.com/atherosclerosis-bulleted-version/view-item?ItemID=72303

2.      http://www.nucleuscatalog.com/acute-coronary-syndrome-and-heart-attack/view-item?ItemID=77416
    Furthermore, i found the AHA ACS algorithm from my sister. I took photos of it:

Picture 5: AHA ACS algorithm 1. Adopted from (AHA, 2011)

Picture 6: AHA ACS algorithm 2. Adopted from (AHA, 2011)

  In this algorithm the main job of the paramedics is to assess and transport the patient. Paramedics must monitor and support the ABCs, administer aspirin, oxygen, nitrates and morphine if needed, and obtain a 12-lead ECG (AHA, 2011).

   Moreover, i read about the AVOID study which found that supplemental oxygen in patients with STEMI without hypoxia, actually increased myocardial injury, recurrent MI, major cardiac arrythmia and larger myocardial infarct size when assessed at six months (Stub, 2012).
   Finally i looked up the ACS CPGs from the JRCALC. They are as follows:

Picture 7: ACS CPG. Adopted from (JRCALC, 2013).

It is also noted in the JRCALC that the treatment of ACS is time-dependent, or as my teacher says "time is myocardium".

References

American Heart Association. (2011). ACLS pocket reference card: Acute coronary syndromes and stroke. Mesquite, TX:American Heart Association.

Desai, R. (Producer & Director). (2012). Atherosclerosis-part1 [video]. U.S.A.: Khan Academy.

Desai, R. (Producer & Director). (2012). Atherosclerosis-part2 [video]. U.S.A.: Khan Academy.
Joint Royal Colleges Ambulance Liaison Committee. (2013). UK ambulance services: Clinical practice guidelines 2013. Bridgwater, England: Class Professional Publishing.

Nucleus Medical Media (2012). Atherosclerosis Bulleted Version. Nucleus Catalog. Retrieved Nov 3, 2015, from http://www.nucleuscatalog.com/atherosclerosis-bulleted-version/view-item?ItemID=72303

Nucleus Medical Media (2015). Acute Coronary Syndrome and Heart Attack. Nucleus Catalog. Retrieved Nov 3, 2015, from http://www.nucleuscatalog.com/acute-coronary-syndrome-and-heart-attack/view-item?ItemID=77416

Stub, D. (2012). A randomized controlled trial of oxygen therapy in acute myocardial infarction Air Verses Oxygen In myocarDial infarction study (AVOID Study). American Heart Journal, 163(3), 339-345. Retrieved from https://my.americanheart.org/idc/groups/ahamah-public/@wcm/@sop/@scon/documents/downloadable/ucm_469664.pdf