Dr. Holliday and class,
PJ’s symptoms are consistent with that of progression to unstable angina. PJ has been diagnosed with stable angina in the past where he is assumed to be taking his ACE inhibitor and nitroglycerin tablets as instructed. PJ also has a history of hypertension which contributes to the hardening and decreased elasticity of his coronary arteries making the progression of his coronary artery disease more likely. PJ also has been experiencing chest pain more frequently with less activity required to cause symptoms to occur. Unstable angina is chest pain that occurs at rest or increases in severity and frequency (McCance & Huether, 2014). This type of chest pain can be excited with minimal exertion and sometimes lasts longer with more intense pain than stable angina. As his provider, I would explain to PJ that his symptoms suggest that he has progressed to unstable angina, what unstable angina is, and despite lack of pain receive emergency medical treatment. Unstable angina is a predecessor to acute MI and indicates that an MI may occur soon (Judd, 2014). If PJ does not have a cardiologist, bringing a cardiologist up-to-date on his condition and treatment is another action I would take. Possible treatments and procedures available to PJ are adding a statin, aspirin, and/or a beta-blocker to his medications and possible angioplasty or coronary artery bypass surgery if medications are no longer a helpful option (Harvard Health Publications, 2015). If PJ is still presenting with chest pain upon arrival to the office, immediate hospitalization is imperative. At the hospital, PJ will have oxygen applied, nitrates given, aspirin given, and morphine given if chest pain is persistent, unless he has experienced allergies to aspirin of morphine in the past (McCance & Huether, 2014).
PJ symptoms and ECG findings are consistent with a STEMI. PJ experienced shortness of breath, severe chest pain that radiated to his jaw and left arm, and he was diaphoretic and pale. His ECG showed significant ST elevation which is consistent with a differential diagnosis of a STEMI. The heart muscle experiencing ischemia will become cooler and cyanotic within 8 to 10 seconds of oxygen deprivation. Immediately, oxygen stores are used and are depleted within 8 seconds because of the heart’s enormous oxygen needs. Anaerobic metabolism begins to provide energy to the myocardium. However, anaerobic metabolism only supplies the cardiac muscle with 65 to 70 percent of the needed energy required for continued function. Because of anaerobic metabolism, hydrogen ions and lactic acid form and collect lowering the pH of the myocardium’s environment. This is harmful to the myocardium since a lower pH increases damage from lysosomal enzymes which restrains the heart’s contractility and impulse conduction functions (McCance & Huether, 2014). Not only does hydrogen and lactic acid build up affect contractility, loss of potassium, calcium, and magnesium electrolytes further damage the heart’s ability to pump. Catecholamines are also released which places the patient in danger of sympathetic and parasympathetic imbalances, irregular heart rhythms, and heart failure (McCance & Huether, 2014). Catecholamines also regulate glycogen, glucose, and stored body fat release. Accumulated fatty acids and glycerol in the plasma can cause deleterious effects on cell membranes. Within one minute of the blocked blood flow, the heart muscle began to experience ischemia or inadequate blood flow (Osmosis, 2016). After 3-5 minutes of occlusion, the ischemic heart muscle stops contracting (McCance & Huether, 2014). After 20-40 minutes, irreversible cardiac damage has been done and a zone of necrosis has formed. Unlike many other cells in the body, cardiac muscle cells do not regenerate after being lost. It is a possibility that because PJ’s heart experienced ischemia on multiple occasions, his heart muscle may be adapted to the oxygen deprivation and preserve heart muscle longer than if he never had angina. The body’s immune system takes over in a several days after an MI causing inflammation. Approximately two weeks after the MI, macrophages begin forming granulation tissue which eventually turns into scar tissue. Scar tissue does not contract and therefore does not assist with blood flow leading to an increased load on other cardiac tissue. This can lead to heart failure in the future (Osmosis, 2016). Cardiac injury can be further exacerbated by reperfusion injury. It is thought that calcium, in the re-established blood flow, causes the injured cells to contract. These cells are unable to relax and are trapped in a contracted state. A return of oxygen can also damage cardiac cells by converting to reactive oxygen species (Osmosis, 2016). In PJ’s case, he would be immediately taken for emergent PCI and antithrombotics.
As far as labs that would indicate PJ having an MI, Troponin I is a determining muscle protein that is released with cardiac damage. It is elevated within 2 to 4 hours upon onset of MI symptoms. It is used to determine MI size and complications that may arise that are linked to the severity of the MI (McCance & Huether, 2014). The CPK-MB, LDH, and CRP are also labs used to assess the patient’s MI severity. Because norepinephrine stimulates the liver and skeletal muscles and suppresses B-cells in the pancreas, blood sugar levels will become elevated within 72 after an MI. This is carefully watched because elevated blood glucose, after an MI, is linked to increased risk for death.
Follow up care after an acute STEMI is important for PJ. He will need to see a cardiologist for cardiac specific care and will likely be started on antiplatelet or blood thinners such as clopidogrel and aspirin to help prevent future MIs. Other medications to improve cardiac perfusion such as a beta-blocker will likely be prescribed.
Harvard Health Publications. (2015). Angina. Retrieved from http://search.proquest.com.southuniversity.libproxy.edmc.edu/docview/1680987719?pq-origsite=summon
Judd, S. J. (2014). Cardiovascular disorders sourcebook (5th ed.). [Adobe Digital Editions]. Retrieved from http://go.galegroup.com.southuniversity.libproxy.edmc.edu/ps/retrieve.do? tabID=&userGroupName=sava2455&inPS=true&prodId=GVRL&contentSet=GALE&docId=GALE|CX3165300020
McCance, K. L., & Huether, S. E. (2014). Pathophysiology: The Biologic basis for disease in adults and children (7th ed.). [Adobe Digital Editions]. Retrieved from https://digitalbookshelf.southuniversity.edu/#/books/9780323088541/cfi/0!/4/2/[email protected]:0.00
Osmosis. (2016, April 30). Heart attack (acute myocardial infarction)- causes, symptoms, types, & pathology [Video file]. Retrieved from https://www.youtube.com/watch?v=GeX7-sxxOn4&feature=youtu.be
Dr. Holliday and fellow classmates,
PJ has had a long history of stable angina which he has been treating with nitroglycerin, an ACE inhibitor, and rest. This regimen has quickly relieved his pain in the past but he has been noticing that his angina has become more frequent with less activity required to initiate the response. The decision to treat PJ’s stable angina with medication and rest was the least invasive treatment and seemed to work for PJ for a long time. If PJ’s physician/NP ordered a stress test for evaluation and it was negative for reversible ischemia, then PJ’s treatment was appropriate. At this point, PJ’s stable angina has become unstable which, worldwide, is the leading cause of death (Solomon & Ohman, 2016). Angina is the clinical manifestation of about half of persons with coronary artery disease (CAD) (Solomon & Ohman, 2016).
Angina is the clinical manifestation of about half of persons with coronary artery disease (CAD) (Solomon & Ohman, 2016). This form of cardiovascular disease is a slow narrowing and stiffening of the wall in arterials (McCance & Huether, 2014). When the body is under stress then the arterials are not able to dilate or contract appropriately to allow sufficient oxygenation and blood pressure causing a buildup of lactic acid and irritates the myocardial nerve fibers resulting in pain (McCance & Huether, 2014). On an electrocardiogram (ECG), ST depression and/or T-wave inversions are characteristic of angina ischemia (McCance & Huether, 2014).
PJ woke up early in the morning with severe chest pain that radiated to his jaw and left arm. He also experienced shortness of breath, diaphoresis, and appeared pale. His wife called the medics and he was transported to the emergency room. The EKG at the emergency room was interpreted as having significant ST- segment elevation. This finding is suggestive of a ST-elevation myocardial infarction (STEMI). Laboratory work to complete would include cardiac troponin I which is the fastest indicator of a MI and should be repeated at 6-9 hours and again ant 12-24 hours (McCance & Huether, 2014). Other tests to complete would include CPK-MB, LDH, and CRP (McCance & Huether, 2014). As well PJs blood glucose level may be increased and can remain high for several weeks following the infarction (McCance & Huether, 2014). In this situation, PJ should be placed on supplemental oxygen, given and aspirin, an ACE inhibitor, morphine sulfate for pain as well as decrease the oxygen demand of the heart muscle, and sent immediately to the catheterization lab for the best possible outcome.
As I wrote in week 1of the Advanced Pathophysiology NSG5003 class on May 19, 2017, “reversible cell injury occurs when the lack of blood flow is short or the cell has an altered state (Unknown Author, no date). The cell will repair itself after the blood flow returns (Unknown Author, no date). Cell death or nonreversible cell injury occurs if lack of blood flow is prolonged, lactate accumulation and anaerobic metabolism sets in causing ATP levels to decrease as well as, intracellular pH (Kalogeris, Baines, Krenz, & Korthuis, 2012). This process causes the ATPase-dependent ions to become dysfunctional which increases mitochondrial and intracellular calcium levels, cell swelling and rupture, and cell death by necrotic, apoptotic, and autophagic mechanisms (Kalogeris et al., 2012). The lack of blood supply to the cells are the initial insult that causes injury or death (Kalogeris et al., 2012). The secondary source of damage and/or cell death is the reperfusion to the area (Kalogeris et al., 2101). The extent of damage depends on the length of time the area is without blood flow (Kalogeris et al., 2012). Approximately 50% of the post infarct is lethal reperfusion injury that results from calcium overload, inflammation, oxidative stress, and rapid pH restoration (Reddy, Khaliq, & Henning, 2015).
Myocardial infarction occurs when blood flow is prolonged to an area of the heart muscle resulting in permanent death of myocytes (Richardson, Clarke, Quinn, & Holmes, 2015). Though some organs, such as the liver can regrow cells, the heart and brain cannot (Unknown Author, no date). Over the next several weeks after the heart muscle dies, scar tissue begins to replace the dead cells (Richardson et al., 2015)”.
(Lithgow, T., 2017)
When the heart undergoes the changes noted above, the cardiac enzyme troponin I level rises in the blood. This enzyme is normally found covering the binding sites of myocin and is bound to actin (McCance & Huether, 2014). In a MI, myocyte necrosis occurs and the heart muscle can sustain reversible or non-reversible damage causing the troponin to be released into the blood stream and will continue to increase over the next several hours. The heart muscle can sustain a blockage for approximately 20 minutes before damage becomes non-reversible or permanent (McCance & Huether, 2014).
PJ may experience left ventricular dysfunction, congestive heart failure, or other myocardial infarction related heart issues depending on the location and severity of tissue death. Close monitoring and extensive education regarding symptom management, medication compliance, exercise, abstinence from smoking, heart healthy diet, signs and symptoms to report, and when to seek emergency care should take place to increase his likelihood of long-term survival.
Kalogeris, T., Baines, C., Krenz, M., & Korthuis, r. (2015). Cell biology of ischemia/reprerfusion injury. International Review of Cell and Molecular Biology, 298, 229-317. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3904795
McCance, K., Huether, S. (2014), Pathophysiology: The Biologic Basis for Disease in Adults and Children, 7th Edition [VitalSource Bookshelf version]. Retrieved from https://bookshelf.vitalsource.com/books/9780323088541
Reddy, K., Khaliq, A., & Henning, R. (2015). Recent advances in the treatment of acute myocardial infarction. World Journal of Cardiology, 7(5), 243-276. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4438466
Richardson, W., Clarke, S., Quinn, T., & Holmes, J. (2015). Physiological implications of myocardial scar structure. HHS Author Manuscripts, 5(4), 1877-1909. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4727398
Solomon, C., & Ohman, E. (2016). Chronic stable angina. The New England Journal of Medicine, 374(12), 1167-1176. Retrieved from https://search-proquest-com.southuniversity.libproxy.edmc.edu/docview/1789078041?accountid=87314
Unknown Author. (No Date). Cellular Injury. Retrieved from http://vet.uga.edu/oldvpp/programs/afvet/attachments/cell_injury_notes.pdf
Discussion 3: Whatever the professor feels like asking. She’s always asking me something. SMH