NRSG353 Acute Care Nursing 2

Question 1

Myocardial infarction is an acute and life-threatening event resulting from a heart disease. It is a persistent bleeding disorder (ischemia) of parts of the heart muscle (myocardium) and is in most cases caused by blood clots in an arteriosclerotically altered constriction of a coronary artery (Thygesen et al., 2007).

The majority of myocardial infarction is caused by coronary heart disease (CHD). Like all acute coronary syndromes in humans, they are almost invariably caused by a sudden lower blood flow in a coronary artery, which is due to arteriosclerotic vascular changes with additional blood clots (coronary thrombosis) and can be accompanied by a convulsive vasoconstriction (coronary spasm) (Nissen & Wolski, 2007).

The resulting disease pattern depends on the localization, the severity and the duration of the circulatory disturbance of the heart muscle.

65-75% of the ST elevation infarcts result from the rupture of a ‘vulnerable’ plaque, i.e. the tear of the thin fibrous cap of an inflammatory altered lipid- rich vessel wall alteration.

When its blood supply is completely interrupted, the heart muscle begins to die after 15-30 minutes. This process of infarction begins on the inside, in the layer facing the heart-chambers, and continues as a function of the outside towards the heart-bag (Nissen & Wolski, 2007).

The major risk factors for myocardial infarction include;

-Tobacco consumption,

-Diabetes mellitus (sugar disease),

-High blood pressure

-Hypercholesterolemia

-Familial exposure

Inherited or acquired disorder of fat metabolism. Above all, increased LDL, elevated IDL, low HDL and elevated triglycerides are problematic (Voight et al., 2012).

 Excessive alcohol consumption increases the risk of myocardial infarction and other serious cardiac diseases.

Some of the risk factors as mentioned earlier are exacerbated by obesity and lack of exercise.

Incidences

The disease affects about 1.2 million Australian citizens. It has been recognized to be the leading cause of death. Myocardial infarction kills an Australian after every 30 minutes. In 2015 alone it caused 12 percent of all deaths (Triant et al., 2007).

Impacts on the patient and family

Myocardial infarction parents are required to reduce their physical activities; therefore, for Mr. Tupa being a parent will not be able to play with his children as expected. This can have a negative impact on the children. He may also be forced to reduce his duties at work something that can lead to reduced income. Therefore, the family may have financial constraints. Some children may also no believe that their father is suffering from myocardial infection and will be on long-term treatment for the disease (Mayou et al., 2008)

Question 2

• Most patients complain of breast pain of varying strength and quality. Typical is an intense pressure sensation behind the thoracic or tightness throughout the chest. Penetrating or tearing pain is also described. The pain can radiate into the arms (more often left), neck, shoulder, upper abdomen, and back. The pain is most often accompanied by dyspnea, nausea, and anxiety. The pain usually has a feeling of indigestion and fullness (Burke & Virmani, 2007).

• Dyspnea- difficulty in breathing in myocardial infarction patients mainly results from the chest pain which makes it difficult for the chest to expand when breathing out. This results in incomplete exhalation and accumulation of carbon dioxide in the lungs raising the blood partial carbon dioxide concentration at the expense of oxygen gas. The patient can suffocate if oxygenation is not done immediately after acute attacks (Canto et al., 2012).
• Arrhythmias- there is pulse irregularities on the frequent extrasystoles during infarction. Heart tissues injured by the infarction are slow in electrical impulse conduction as compared to unaffected heart tissues. This difference in conduction velocity elicits a feedback loop that results in many lethal pulse rhythm irregularities. The most common arrhythmias include ventricular tachycardia which causes rapid heart rates preventing the heart from beating normally, and ventricular fibrillation (Nissen & Wolski, 2007).
• In auscultation, in addition to the two normal heart tone, a third heart tone and rattling noises over the lungs as well as cervical congestion on a pump is heard. This shows the weakness of the heart often indicating heart failure. This can further be confirmed by the poor body tissue perfusion as there is a low pulse rate. Body tissues are therefore not supplied with sufficient nutrients such as oxygen and nutrients and accumulation of wastes such as carbon dioxide can lead to death especially when major body organs e.g. the brain are affected (Skyschally et al., 2008).
• Myocardial infarction most commonly occurs in the morning, and this can be related to morning elevated sympathetic tone causing increased blood pressure, coronary vascular tone, heart rate and myocardial contractility thereby leading to an increase in myocardial demand. Increasing myocardial demand elicits the chest pain which may worsen the respiratory rates hence emergency interventions are recommended (Burke & Virmani, 2007).

Question 3

1. Thrombolytics

Thrombolysis (also known as fibrinolysis) means dissolving a blood clot and used as a term for a medical treatment given to patients with blood clots in, for example, the brain, heart or lungs. It works by stimulating the degradation of the fibrin clot by providing an infusion of an analog to tPA (tissue plasminogen activator), which is the protein in the blood that typically activates plasmin. An example of these drugs includes; Streptokinase, Alteplase, Reteplase, and Tenecteplase (Steg et al., 2012).

A blood clot is formed by adhering the platelets to a lump while simultaneously forming fibrin via the coagulation process. Fibrin is a non-water-soluble protein that forms a network and clamps the blood clot so that it does not fall apart.

This mechanism ensures that holes in blood vessels are quickly closed so that bleeding can be stopped. Once the blood clot has worn its purpose, the enzyme is secreted tPA (tissue plasminogen activator) which converts the inactive plasminogen into the blood to the plasma. Plasmin will then break down the fibrin network and cause the blood clot to dissolve. In thrombolysis, it is this natural process that one seeks to accelerate by administering tPA earlier than normal. Thus, the plasma in the blood becomes activated immediately, and the blood clot is dissolved before the affected tissue dies (Van de Werf et al., 2008). These drugs are very useful in patients with acute myocardial infarction where balloon expansion is not possible. The drug should be given within 12 hours.

1. Antiplatelet agents

A platelet antiaggregant is a drug that decreases platelet aggregation and inhibits thrombus formation. Anti-aggregates are useful in the arterial circulation, where anticoagulants have little effect. They are often used in the primary and secondary prevention of cerebrovascular or cardiovascular thrombotic diseases, such as acute coronary syndrome, the thrombotic complication of an atheroma of the coronary arteries (Van de Werf et al., 2008). Examples include;

-Aspirin causes an irreversible inhibition of this enzyme, resulting in the decrease of thromboxane-A2.

-Clopidogrel, Ticlopidine, Prasugrel and Dipyridamole.

Besides the risks specific to each molecule, they increase the risk of hemorrhage, whether spontaneous or during an intervention. The combination with anticoagulants should be particularly careful. A dual therapy also increases the risk (Steg et al., 2012).

Question 4

The nurse initially focuses on the most rapid detection of acute danger and complications. This includes a quick clinical examination with blood pressure measurement and auscultation of the heart and lung (Reichlin et al., 2009). Only a fast-paced twelve-channel ECG reveals the ST-stroke infiltration and allows the initiation of the then urgent lysis therapy or catheter treatment. To be able to detect cardiac arrhythmias immediately, continuous ECG monitoring (rhythm monitoring) is started, and a peripheral dwell cannula is applied for medication delivery (Prasad et al., 2008).

In the acute situation, the drug therapy aims at the best possible oxygen supply to the heart, the pain control and the prevention of further blood clot formation. As a rule, nitroglycerin spray or capsules are administered sublingually and morphine preparations, acetylsalicylic acid, and clopidogrel as well as heparin intravenously. According to the current guidelines of the WHO, oxygen is delivered only at low oxygen saturation of the blood. The general use of oxygen should be well monitored because of its possibly harmful effects. It is only recommended for patients with respiratory distress (Prasad et al., 2008).

In special situations and complications more medications may be needed to calm ( sedation ), for example, benzodiazepines , such as diazepam or midazolam in vagal reaction atropine , nausea or vomiting antiemetics (e.g., metoclopramide ), with tachycardia despite pain relief and missing signs of left heart failure beta-blockers ( for example, metoprolol ) and in cardiogenic shock the administration of catecholamines .

The primary aim of the ST-stroke infiltration is to open the affected coronary vessel, which is mostly occluded in this situation, as quickly as possible. This restoration of the blood flow in the infarction area is called reperfusion therapy. The earlier this is done, the better can be an infarct expansion. If it is possible to use reperfusion therapy already in the first hour after infarction, many of these infarctions can even be prevented. The nurse can then participate in reperfusion therapy or refer the patient for percutaneous coronary intervention which can be done in one of these two ways;

• Primary percutaneous coronary intervention (also direct PTCA or primary PTCA): mechanical opening (recanalization) of the vessel followed by balloon dilatation and stent implantation using a cardiac catheter. If a result which is not applicable using PTCA is shown, an acute operative myocardial revascularization may be indicated in individual cases (Ellis et al., 2008).
• Lysetherapy or thrombolysis: intravenous administration of a medicament that dissolves clot. This thrombolytic agent can of emergency be administered already at the site and runs through early initiation of treatment to better results than therapy initiation in the hospital.

In the hospital, infarction patients are treated for acute cardiac arrhythmia in the acute phase at an intensive care or monitoring station, where continuous ECG monitoring is possible. This helps reduce myocardial workload thereby preventing exacerbations of the disease (Kramer et al., 2008).

Patient management in emergency situations is quite difficult and requires interdisciplinary approach. A close working relationship between nurses and other healthcare providers such as medical practitioners and pharmacists should be encouraged. This is important in quick action in attempts to save the patient.

References

Burke, A. P., & Virmani, R. (2007). Pathophysiology of acute myocardial infarction. Medical Clinics of North America, 91(4), 553-572.

Canto, J. G., Rogers, W. J., Goldberg, R. J., Peterson, E. D., Wenger, N. K., Vaccarino, V., … & NRMI Investigators. (2012). Association of age and sex with myocardial infarction symptom presentation and in-hospital mortality. Jama, 307(8), 813-822.

Ellis, S. G., Tendera, M., De Belder, M. A., Van Boven, A. J., Widimsky, P., Janssens, L. & Peruga, J. Z. (2008). Facilitated PCI in patients with ST-elevation myocardial infarction. New England Journal of Medicine, 358(21), 2205-2217.

Kramer, M. C., van der Wal, A. C., Koch, K. T., Ploegmakers, J. P., van der Schaaf, R. J., Henriques, J. P., … & Tijssen, J. G. (2008). Presence of older thrombus is an independent predictor of long-term mortality in patients with ST-elevation myocardial infarction treated with thrombus aspiration during primary percutaneous coronary intervention. Circulation, 118(18), 1810-1816.

Kushner, F. G., Hand, M., Smith, S. C., King, S. B., Anderson, J. L., Antman, E. M., … & Green, L. A. (2009). 2009 Focused Updates: ACC/AHA Guidelines for the Management of Patients With ST?Elevation Myocardial Infarction (Updating the 2004 Guideline and 2007 Focused Update) and ACC/AHA/SCAI Guidelines on Percutaneous Coronary Intervention (Updating the 2005 Guideline and 2007 Focused Update). Catheterization and Cardiovascular Interventions, 74(7).

Mayou, R., Foster, A., & Williamson, B. (2008). The psychological and social effects of myocardial infarction on wives. Br Med J, 1(6114), 699-701.

Nissen, S. E., & Wolski, K. (2007). Effect of rosiglitazone on the risk of myocardial infarction and death from cardiovascular causes. New England Journal of Medicine, 356(24), 2457-2471.

O’Gara, P. T., Kushner, F. G., Ascheim, D. D., Casey, D. E., Chung, M. K., De Lemos, J. A., … & Granger, C. B. (2013). 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction. Circulation, 127(4), e362-e425.

Prasad, A., Lerman, A., & Rihal, C. S. (2008). Apical ballooning syndrome (Tako-Tsubo or stress cardiomyopathy): a mimic of acute myocardial infarction. American heart journal, 155(3), 408-417.

Reichlin, T., Hochholzer, W., Bassetti, S., Steuer, S., Stelzig, C., Hartwiger, S. & Noveanu, M. (2009). Early diagnosis of myocardial infarction with sensitive cardiac troponin assays. New England Journal of Medicine, 361(9), 858-867.

Skyschally, A., Schulz, R., & Heusch, G. (2008). Pathophysiology of myocardial infarction. Herz, 33(2), 88-100.

Steg, P. G., James, S. K., Atar, D., Badano, L. P., Lundqvist, C. B., Borger, M. A., … & Gershlick, A. H. (2012). ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. European heart journal, ehs215.

Thygesen, K., Alpert, J. S., & White, H. D. (2007). Universal definition of myocardial infarction. Journal of the American College of Cardiology, 50(22), 2173-2195.

Triant, V. A., Lee, H., Hadigan, C., & Grinspoon, S. K. (2007). Increased acute myocardial infarction rates and cardiovascular risk factors among patients with human immunodeficiency virus disease. The Journal of Clinical Endocrinology & Metabolism, 92(7), 2506-2512.

Van de Werf, F., Bax, J., Betriu, A., Blomstrom-Lundqvist, C., Crea, F., Falk, V. & Rosengren, A. (2008). Management of acute myocardial infarction in patients presenting with persistent ST-segment elevation. European heart journal, 29(23), 2909-2945.

Voight, B. F., Peloso, G. M., Orho-Melander, M., Frikke-Schmidt, R., Barbalic, M., Jensen, M. K., & Schunkert, H. (2012). Plasma HDL cholesterol and risk of myocardial infarction: a mendelian randomisation study. The Lancet, 380(9841), 572-580.