Antero-septal Myocardial infarction assessment

Cardiology Nursing

This is a 12 lead ECG taken for Mr. Long at the Emergency Department. He presented with a two hour history of chest pain radiating to his left arm. The ECG is suggestive of an antero-septal Myocardial infarction. Further scrutiny of the ECG displays a normal sinus rhythm, with a rate of 75 bpm that is regularly regular. There is no axis deviation with a PR interval of 200 ms and normal qrs complexes. Leads I and aVL also show a q wave which may be suggestive of an old high lateral wall MI. Leads I, V1, V2, V3 and aVL show ST segment elevation of greater than 2 mm and ST segment depression in leads II and III. Mr. Long is suffering from a fully evolved ST-segment elevation myocardial infarction.

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A correlation can be made with the area of myocardium involved and the vessel involved. The antero-septal wall is supplied by the Left Anterior Descending. A blockade in this branch may manifest as an anterior wall, septal, antero-septal or an extensive anterior wall MI. The LAD artery originates from the left coronary artery. A blockade in the Left coronary artery would also affect the circumflex branch which does not seem to be the case in Mr. Long’s ECG. (Boon, Colledge, Walker & Hunter, 2010)

The LAD artery runs along the anterior interventricular sulcus and supplies the apical portion of both ventricles. (Boon et al., 2010) When the myocardium, which is supplied by the LAD artery, dies; the conduction from the AV node to the bundle of His and purkenje fibers will be impaired, generating possible ectopic focuses, leading to ventricular arrhythmias.

Other complications of Myocardial infarction can be classified as early (when occurring within the first 2-3 days), later and late complications. Early complications include cardiac arrhythmias, cardiac failure and pericarditis. Amongst the later complications are recurrent infarction, angina, thromboembolism, mitral valve regurgitation, ventricular septal defect and cardiac rupture. Post myocardial infarction syndrome, shoulder hand syndrome, ventricular aneurysm and recurrent cardiac arrhythmias are late complications of a myocardial infarction. (Boon et al., 2010)


When considering treatment for myocardial infarction, the duration of symptoms is an important factor. The focus of most current literature is on reducing the time it takes for a patient with ST-segment elevation myocardial infarction, STEMI, to receive fibrinolytics or undergo Primary PCI. The current recommendation by the American College of Cardiology / American Heart Association, ACC/AHA, is to initiate reperfusion with fibrinolytics within 30 minutes or to perform Primary PCI within 90 minutes of presentation to the Emergency Department. (Diercks, 2010)

The mode of treatment of STEMI patients differs for those arriving to a PCI-capable facility from those arriving to a PCI-referral center. The time duration for initial management and transfer needs to be estimated before referral. This requires a carefully planned STEMI protocol system. (Diercks, 2010)

Measures for initial management include reducing activity, stopping any form of oral intake for the first 4-12 hours, making a bedside commode facility available and giving laxatives if there is constipation, sedation and starting Oxygen supplementation if the oxygen saturation is low. (Boon et al., 2010)

Patient activity is reduced to bed rest for the first 12 hours, then sitting upright within 24 hours. If there is no hypotension, the patient is allowed to ambulate in his room on the third day. The level of activity is progressively increased from the fourth day onwards to a goal of 600 feet at least 3 times daily, if no complications exist. Pain control can be successfully achieved with a combination of nitrates, morphine, oxygen and beta-blockers. An IV cannula should be inserted and 4-8 mg morphine plus cyclizine (Marzine 50 mg) can be used every 5-15 minutes until the pain is relieved or there is evidence of morphine toxicity, such as, hypotension, respiratory depression or severe vomiting. In this case, atropine, 0.5-1.5 mg IV, and naloxone, 0.1-0.2 mg IV can be used to combat hypotension and respiratory depression. (Boon et al., 2010)

The current recommended dose of Aspirin is 300 mg, initially, that should be given in a soluble or a chewable form. The subsequent doses should 75-300 mg daily. Clopidogrel or Prasugrel can be given in conjunction with aspirin in a dose of 300-600 mg for Clopidogrel and 60 mg for Prasugrel. Prasugrel has proven to have a 19% relative risk reduction in the primary efficacy endpoint. The use of GP II a / III b inhibitors has also proven beneficial through many clinical trials and the current guidelines recommend its use before primary PCI. (Jois, 2011)

Options for intravenous anticoagulant therapy include bivalirudin, intravenous unfractionated heparin (UFH), enoxaparin, and fondaparinux. (Jois, 2011) When treating patients with unfractionated heparin, additional boluses may be given to maintain therapeutic clotting time levels. IV heparin should be continued for at least 24 hours after thrombolytic therapy with tPA but is not recommended for patients receiving streptokinase. The dose of heparin should be 5000 units IV bolus followed by 1000 units per hour IV infusion. On the other hand, patients who do not receive thrombolytic therapy, the dose of heparin should be 7500 units S/C, 12 hourly until the patient is ambulatory. (Boon et al., 2010)

Drugs given for thrombolysis include Streptokinase, Altepase, Reteplase, Tenecteplase. Altepase, Reteplase and Tenecteplase are recombinant tissue plasminogen activators (t-PA). Streptokinase is given in a dose of 1.5 million units in 100 ml of saline, IV, over one hour. With streptokinase, there is no need to give heparin. Streptokinase has the disadvantage of causing allergic reactions and severe hypotension if infused rapidly. Altepase is given as a 15 mg bolus followed by 50 mg over the next 30 minutes and then 35 mg over the following 60 minutes. IV heparin is recommended for at least 24 hours when using a t-PA. Although Altepase does not cause allergic reactions or hypotension, it has the disadvantage of being more expensive. It has also been associated with a greater risk of intracranial hemorrhage, than other fibrinolytics, especially in patients with hypertension and in those greater than 70 years. (Boon et al., 2010)

Intravenous nitroglycerine is not used in all patients of MI because recent trials have shown no survival benefit from its routine use following MI. However, it is indicated in patients with left ventricular failure due to MI, hypertensive patients, recurrent or persistent ischemic pain and in high risk patients, especially those with a large anterior wall MI. In such patients, IV nitrates are used for the first 24-48 hours. (Boon et al., 2010)

Acute beta blockade reduces the risk of complications after an MI, for example, cardiac rupture and ventricular arrhythmias. It also decreases ischemic chest pain and infarct size. Metoprolol is given IV every 5 minutes for 3 doses, provided that the heart rate does not fall below 60 bpm and that the systolic blood pressure does not drop below 100 mmHg. After this, maintenance dose is started with metoprolol, orally, 50 mg, every 6 hours for 2 days and then 100 mg twice daily. (Boon et al., 2010)

Angiotensin Converting Enzyme Inhibitors prevent left ventricular dilatation and cardiac failure and should be given to all hemodynamically stable patients with in the first 24 hours and should be continued, for the whole life, in high risk MI patients. Captopril is given as an initial dose for 6.25 mg and then increased every 6-8 hours to a maximum of 50 mg, 3 times daily provided that the systolic blood pressure is maintained beyond 100 mmHg. (Boon et al., 2010)

Mr. Long was continued with Oxygen and was given Aspirin and Clopidogrel, as consistent with current recommendations. However, with an elevated blood pressure and a pulse rate of 90 bpm, Beta blockers and ACE inhibitors would have been ideal. On examination, Mr. Long appeared anxious and so IV morphine was initiated to reduce pain and anxiety. IV nitroglycerine could also be given, since Mr. Long was suffering from a large anterior wall MI. Timely use of fibrinolytics is the treatment of choice if the patient is at a non-PCI center and heparin is recommended if the patient is not receiving streptokinase. The new class II recommendation considers the transfer or patients at a non-PCI facility to a PCI facility as soon as possible, after the use of thrombolytics. (Jois, 2011)

Minimizing door to balloon and door to needle times is crucial and requires successful coordination of multiple complex processes under the control of different staff. The multidisciplinary approach is a collaborative effort of the emergency department and PCI lab physician and nursing leadership to improve the care of STEMI patients and includes the following steps mentioned below.

The receiving resident or nursing staff should admit the patient in a quite environment where continuous ECG and hemodynamic variables can be monitored. There should also be easy access to defibrillator facilities. Nursing care should be provided by individuals trained in critical care. Once the 12 leads are attached and an IV line is maintained, a 12 lead ECG should be obtained, interpreted and conveyed to the on-call resident or cardiologist. Vitals and oxygen saturation should also be monitored simultaneously. Initial Labs include cardiac markers and blood CP/ESR. An X-ray of the chest and an echocardiography are also performed. (Kaplow & Hardin, 2003)

After the initial management, the patient should be monitored continuously for ECG changes, vitals and oxygen saturation. If the patient remains stable for 6 hours, the need for oxygen should be re-assessed and discontinued if above 98%. hypotension and respiratory depression should be monitored as side-effects of morphine. APTT and INR are performed at regular intervals to monitor the therapeutic dosages of thrombolytics. (Kaplow & Hardin, 2003)


Myocardial oxygen demand can be decreased by decreasing heart rate, contractility, ventricular afterload, and ventricular preload. Because the heart is being stimulated by increased sympathetic activity and circulating catecholamines during an infarction, drugs such as beta-blockers and ACE inhibitors help reduce heart rate, afterload and preload. (Katzung & Masters, 2011)

ACE inhibitors act by inhibiting the conversion of Angiotensin I to Angiotensin II. Angiotensin II is a potent vasoconstrictor and promotes the production of aldosterone. Aldosterone causes water retention by promoting sodium reabsorption in the kidneys. This increases the volume inside blood vessels. By inhibiting the enzyme, ACE, angiotensin II is not produced. This causes vasodilation and decreases the preload. (Katzung & Masters, 2011)

Preload is the load or pre-stretch on the ventricular muscle at the end of diastole. The pre-load can be measured through several indices. The left ventricular end-diastolic volume and left ventricular end diastolic pressure are indicators of the preload on the left ventricle. Less reliable indices or left ventricular preload are those measured in the venous system. These include: left atrial pressure, pulmonary venous pressure and pulmonary wedge pressure. (Katzung & Masters, 2011)

The vasodilation properties of ACE inhibitors also help in reducing the after load. The afterload is a measure of the force that the myocardium must exhibit to spill the blood into the aorta. The mean aortic pressure, peak left ventricular pressure and the ejection fraction are measures of the afterload. (Katzung & Masters, 2011)

ACE inhibitors cause vasodilation by blocking the action of angiotensin II and inhibits bradykinin metabolism. Bradykinin is a vasodilator. Angiotensin II also activates the sympathetic system which is blocked by ACE inhibitors. (Katzung & Masters, 2011)

One of the important use of ACE inhibitors in MI stems from its ability to inhibit cardiac and vascular remodeling, which is associated with chronic hypertension, heart failure, and myocardial infarction. (Katzung & Masters, 2011)

Beta blockers are recommended for use during the management of an MI. Beta blockers act by inhibiting sympathetic activation of the heart in response to increased catecholamines during an MI. Increased heart rate in response to increased sympathetic activity is associated with poor prognosis of MI patients. Studies have also displayed a relationship with heart rate and hospital mortality, as well as 6-month mortality, in patients with MI. (Katzung & Masters, 2011)

Beta blockers also improve autonomic imbalance, which is the variability of heart rate due to increased sympathetic tone and reduced vagal tone during exersize. Beta blockers also increase left ventricular ejection fraction, reduce end-systolic volume, thus improving cardiac filling and ejection fraction. Like ACE inhibitors, beta blockers also prevent cardiac remodeling, when used in long-term. ACE inhibitors prevent cardiac remodeling by inhibiting progressive left ventricular dilatation, whereas, beta blockers reverse the re-modelling process by reducing left ventricular volumes and by improving systolic functions. (Katzung & Masters, 2011)


The ABG values show acidosis and low oxygen saturation. Since, both carbon dioxide and bicarbonate values reflect academia, a mixed disorder is most likely. Further analysis of electrolytes will help determine the type of the mixed disorder present. The ABG analysis and the Chest X-ray along with signs and symptoms suggest that Mr. Long is developing congestive cardiac failure.

To maintain Mr. Long’s oxygen saturation, non-invasive options for respiratory support include: intermittent positive pressure ventilation (IPPV), controlled mandatory ventilation (CMV), synchronized intermittent mandatory ventilation (SIMV), pressure controlled ventilation (PSV), pressure support ventilation (PSV), positive end expiratory pressure (PEEP), bilevel positive airway pressure (BiPAP), continuous airway pressure (CPAP) and Non-invasive intermittent positive pressure ventilation (NIPPV). This ventilator support can be achieved through a mouth piece or nasal, face or helmet mask. (Boon et al., 2010)

The objective of any strategy used is to improve gas exchange, minimize lung damage by avoiding high lung volumes and FIO2, avoid adverse circulatory effects, and to make the patient as comfortable as possible by reducing the work of breathing. To rationalize which mode of support to use, it is important to first assess Mr. Long’s condition. In this scenario, Mr. Long has developed pulmonary edema. (Boon et al., 2010)

Simple supplementation of added oxygen will not help Mr. Long’s hypoxemia. This is because of fluid accumulation in the lungs which require an increased pressure, therefore an increased work load, to force air through the fluid into the alveoli. Pressure supported ventilation, therefore, would be the ideal choice of support. These include, SIMV, CPAP and BiPAP. PEEP, even though an option in pulmonary edema, it cannot be used in this case because of its ability to hamper venous return and reduce cardiac output. The clinical scenario is also not favorable towards the use of PSV since PSV only provides positive pressure to augment patient’s breaths. With severe pulmonary edema, an increased work load is required to deliver oxygen to the alveoli which cannot be relieved with PSV. (Boon et al., 2010)

The recommended management of respiratory assistance in pulmonary edema is to give oxygen in a high flow and concentration through CPAP, of 5-10 mmHg, by a tight fitting mask. Studies have revealed that even though both CPAP and BiPAP have been associated with a significant reduction in the need for mechanical ventilation, BiPAP has shown to cause a non-significant increase in risk for myocardial infarction. (Moloo, 2006)

In BiPAP, the inspiratory phase of the respiratory cycle (IPAP) is set higher than the expiratory phase (EPAP). A common setting would be IPAP of 12 cm and EPAP of 6 cm. At no time does the airway pressure return to zero. In CPAP, the patient breathes through a pressurized circuit against a threshold resistor that keeps the airway pressure at a preset level. To qualify as CPAP, both the inspiratory and expiratory pressures must be the same. CPAP is known to lessen dyspnea by improving the pathophysiology of heart failure in two general areas: pulmonary mechanics and hemodynamics. (Boon et al., 2010)

CPAP is ideal because it recruits alveoli, increases functional residual capacity, and allows breathing on the more compliant portion of the lung’s pressure-volume curve, thereby decreasing the work of breathing, improving ventilation-perfusion relationships, and eventually correcting hypoxemia, hypercapnia and therefore, acidemia. Positive intrathoracic pressure also decreases preload and left ventricular afterload, both beneficial effects in patients with volume overload. BiPAP also produces the same physiological improvements as CPAP, but its use in cardiac failure is controversial. (Boon et al., 2010)

Common side effects of CPAP and BiPAP include dizziness, headaches, rhinitis and gastrointestinal problems. Mask CPAP discourages coughing and clearing of lung secretions, which may cause aspirations. (Boon et al., 2010)

As a critical care nurse, it is important to be able to assess for signs and symptoms of ineffective breathing patters and to implement measures to improve breathing. General measures would be to place the patient in an upright position, since patients with pulmonary edema feel respiratory comfort in this position. The patient must be kept pain free and actions need to be taken to reduce patient anxiety and fear. All forms of oral intake and IV fluids need to be either stopped or given in minute amounts. It is also the duty of a nurse to assist with positive airway pressure techniques and monitor respiratory variables. The patient needs to observe complete bed rest until his condition improves. In case of decreased respiratory derive, declining oxygen saturation or development of signs of cardiogenic shock, the appropriate health care provider needs to be consulted. (Kaplow & Hardin, 2003)


Despite management, Mr. Long’s status progressively deteriorated and he developed cardiogenic shock. This was manifested by tachypnea, altered mental status, decreased blood pressure, oxygen saturation and peripheral perfusion; raised JVP and pulmonary crackles.

For the purpose of management, shock is divided into three stages. The first is an initial, non-progressive stage, during which compensatory mechanisms are activated that maintains perfusion to vital organs. The next stage is characterized by tissue hypoperfusion and worsening circulatory and metabolic imbalance. At this stage of his clinical situation, Mr. Long is in the second stage of shock. The second stage can progress to an irreversible stage at which time considerable cellular and tissue injury has occurred. (Kumar & Robbins, 2007)

The pathophysiology behind the cardiogenic shock in Mr. Long is cardiac failure leading to fluid overload. A reduced cardiac output causes neurohumoral activation, which includes sympathetic activation as well as the renin-angiotensin, vasopressin and endothelin system. This causes vasoconstriction in the peripheral vessels, increasing blood pressure and afterload. The heart, therefore, must work harder. Activation of the renin-angiotensin system also causes sodium and water retention, increasing intravascular volume, blood pressure and cardiac work. All of these factors combine to cause myocyte loss, further potentiating heart failure. (Kumar & Robbins, 2007)

With increasing ventricular dysfunction, there is an increase in the left ventricular diastolic pressure which increases backflow congestion in the pulmonary vasculature, causing hypoxia. Systolic dysfunction decreases cardiac output and blood pressure, which in turn decreases coronary perfusion. Hypoxia, due to pulmonary edema, and decreased coronary perfusion causes further ischemia which further decreases ventricular dysfunction. (Kumar & Robbins, 2007)

Eventually, a point is reached when there is critical impairment of tissue perfusion that can no longer be compensated for by neurohumoral activation. Poor tissue perfusion causes end-organ damage. Decreased perfusion to the brain can lead to altered mentation and even brain death. The brain is particularly sensitive to hypoxia and so altered mental status occurs early in shock. Hypoxia to the gastrointestinal tract can cause infarction of the bowels, which can lead to fluid and electrolyte imbalances and acidosis. Patchy mucosal hemorrhages and necrosis occur. This particular change is referred to as hemorrhagic enteropathy. (Kumar & Robbins, 2007)

The effect of shock in the kidneys can cause “pre-renal” acute renal failure. Ischemia of the tubule epithelium causes Acute Tubular Necrosis due to decreased perfusion. This causes decreased glomerular filtration rate, oliguria, and azotemia. Centrilobular necrosis in the liver is not a common consequence of pure cardiogenic shock. However, it does occur commonly in septic shock. There is diminished reticuloendothelial clearance, intrahepatic cholestasis and elevated bilirubin. (Kumar & Robbins, 2007)

Decreased perfusion in the lungs causes the pulmonary vessels to become leaky, further exacerbating interstitial edema and causing hyalinization and decreased compliance. Reduced lung compliance causes a decrease in ventilation, leading to respiratory acidosis. At the same time, there is a very high oxygen consumption and carbon dioxide production. As a result, there is ventilation perfusion mismatch, shunting of blood and pulmonary hypertension, all leading to severe hypoxemia, causing lactate levels to rise. Lactate levels directly correlate with mortality. (Kumar & Robbins, 2007)

Adrenal changes in shock are seen as an equal recurrence in all forms of shock. The major change is cortical cell lipid depletion. This change does not reflect adrenal insufficiency but rather conversion of the relatively inactive vacuolated cells to metabolically active cells that store and utilize lipids for the synthesis of steroids. (Kumar & Robbins, 2007)

With the exception of neuronal and myocyte loss, all the other tissue changes can revert to normal before the irreversible stage, if patients survive the initial insult. Unfortunately, deterioration is rapid and patients usually succumb before the tissues get an opportunity to recover. Moreover, secondary complications may occur in patients who recover from the initial stress. This stage is dominated by renal insufficiency causing severe fluid and electrolyte imbalance. The prognosis of Mr. Long according to current literature is slim. Cardiogenic shock secondary to myocardial infarction is associated with a mortality rate of 70%-80%, even with the best care available. (Kumar & Robbins, 2007)


B, Deborah, Diercks. (2010). Mission Lifeline: Developing a STEMI regonal care. American Heart Association. -. Print.

Jois, P. (2011). Nstemi and stemi: therapeutic updates 2011. The Practical Journal for Emergency Physicians, 32(1), 1-7.

Katzung, B., & Masters, S. (2011). Katzung’s pharmacology. (9 ed.). United States of America: Mc-Graw Hill.

Kumar, V., & Robbins, (2007). Basic pathology. (8 ed.). London: Saunders Company.

Nicholas A. Boon, Nicki R. Colledge, Brian R. Walker, John A.A. Hunter.(2010). Davidson’s Principles and Practice of Medicine . India, Elsevier.

Roberta, K., & Sonya, H. (2003). Critical care nursing: Synergy for optimal outcomes. (pp. 197-209). Boston: Jones & Bartlett Publishers.

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