Cardiac Case Study Nursing Students

1. Remes J, Miettinen H, Reunanen A, Pyorala K. Validity of diagnosis of heart failure in primary health care. Eur Heart J. 1991;12:315–321.[PubMed]

2. Gillespie ND, McNeill GP, Pringle TH, Ogston S, Struthers AD, Pringle SD. Cross sectional study of contribution of clinical assessment and simple cardiac investigations to diagnosis of left ventricular systolic dysfunction in patients admitted with acute dyspnoea. Br Med J. 1997;314:936–940.[PMC free article][PubMed]

3. Davie AP, Francis CM, Love MP, et al. Value of the electrocardiogram in identifying heart failure due to left ventricular systolic dysfunction. Br Med J. 1996;312:222–224.[PMC free article][PubMed]

4. Dargie HJ, McMurray JVV. Diagnosis and management of heart failure. Br Med J. 1994;308:321–328.[PMC free article][PubMed]

5. Badgett RG, Mulrow CD, Otto PM, Ramirez G. How well can the chest radiograph diagnose left ventricular dysfunction? J Gen Int Med. 1996;11:625–634.[PubMed]

6. Choy AM, Darbar D, Lang CC, et al. Detection of left ventricular dysfunction after myocardial infarction: comparison of clinical, echocardiographic and neurohormonal methods. Br Heart J. 1994;72:16–22.[PMC free article][PubMed]

7. Raftery EB. Haemodynamic effects of diuretics in heart failure. Br Heart J. 1994;72(suppl S):44–S47.[PMC free article][PubMed]

8. Verma SP, Silke B, Hussain M, et al. First line treatment of left ventricular failure complicating acute myocardial infarction: a randomised evaluation of immediate effects of diuretic, venodilator, arteriodilator and positive inotropic drugs on left ventricular function. J Cardiovasc Pharmacol. 1987;10:38–46.[PubMed]

9. Collins R, Peto R, Flather M for the ISIS4 Study Group. A randomised factorial trial assessing early oral captopril, mononitrate or intravenous magnesium sulphate in 58 050 patients with suspected acute myocardial infarc 321–328tion. Lancet. 1995;345:669–685.[PubMed]

10. Flynn K, Coughlan MG, Phelan DM, Luke D, Neligan M, Wood AE. Intravenous captopril in acute heart failure. Lancet. 1988;301:173–174.[PubMed]

11. Swedberg K on behalf of the CONSENSUS Trial investigators. Effects of early administration of enalapril on mortality in patients with acute myocardial infarcation—results of the cooperative new scandinavian study II (CONSENSUS II) N Engl J Med. 1992;327:678–684.[PubMed]

12. Annane D, Bellisant E, Pussard E, et al. Placebo controlled, randomized double blind study of intravenous enalaprilat efficacy and safety in acute cardiogenic pulmonary edema. Circulation. 1996;94:1316–1324.[PubMed]

13. Garg R, Yusuf S. Overview of randomized trials of angiotensin converting enzyme inhibitors on mortality and morbidity in patients with heart failure. J Am Med Ass. 1995;273:1450–1456.[PubMed]

14. Hillis GS, Trent RJ, Winton P, MacLeod AM, Jennings KP. Angiotensin converting enzyme inhibitors in the management of cardiac failure: are we ignoring the evidence? Quart J Med. 1995;89:145–150.[PubMed]

15. Hart W, Rhodes G, McMurray J. The cost effectiveness of enalapril in the treatment of chronic heart failure. Br J Med Econ. 1993;6:91–98.

16. Benedict CR, Francis GS, Shelton B, et al. Effect of long term enalapril therapy on neurohormones in patients with left ventricular dysfunction. Am J Cardiol. 1995;75:1151–1157.[PubMed]

17. Cleland JGF, Poole-Wilson PA. ACE inhibitors for heart failure a question of dose. Br Heart J. 1994;72:s106–s110.[PMC free article][PubMed]

18. Poole Wilson PA The NETWORK Study—The effect of dose of an ACE inhibitor on outcome in patients with heart failure. Heart. 1996;75(s1):95.

19. Packer M. Do angiotensin converting enzyme inhibitors prolong life in patients with heart failure treated in clinical practice. J Am Coll Cardiol. 1996;28:1323–1327.[PubMed]

20. Pfeffer MA for the SAVE Study Investigators. Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infarction. N Engl J Med. 1992;327:669–677.[PubMed]

21. Grinstead WC, Francis MJ, Marks GF, Tawa CB, Zoghbi WA, Young JB. Discontinuation of chronic diuretic therapy in stable congestive heart failure secondary to coronary artery disease or to idiopathic dilated cardiomyopathy. Am J Cardiol. 1994;73:881–886.[PubMed]

22. Rongen GA, Lenders JWM, Smits P, Thein T. Clinical pharmacokinetics and efficacy of renin inhibitors. Clin Pharmacokin. 1995;29:6–14.[PubMed]

23. MacFadyen RJ, Jones CR, Doig JK, Birnbock H, Reid JL. Responses to an orally active renin inhibitor remikiren (Ro-42-5892) after controlled salt depletion in humans. J Cardiovasc Pharmacol. 1995;25:347–353.[PubMed]

24. MacFadyen RJ. Angiotensin receptor antagonists from theory to practice. In: Elliott HL, editor. Current issues in cardiovascular therapy. London: Martin Dunitz; 1997. pp. 35–51. chapter 3.

25. Lacourciere Y, Brunner HR, Irwin R, et al. Effects of modulators of the renin angiotensin system on cough. J Hypertension. 1994;12:1387–1393.[PubMed]

26. Pitt B, Segal R, Martinez FA, et al. Randomized trial of losartan versus captopril in patients over 65 with heart failure (Evaluation of losartan in the elderly Study, ELITE) Lancet. 1997;349:747–752.[PubMed]

27. Gohlike P, Linz W, Scholkens BA, et al. Angiotensin converting enzyme inhibition improves cardiac function: role of bradykinin. Hypertension. 1994;23:411–418.[PubMed]

28. Cohn JN, Archibald DG, Ziesche S, et al. Effect of vasodilator therapy on mortality in chronic congestive heart failure: results of a Veterans Administration Cooperative Study. N Engl J Med. 1986;314:1547–1552.[PubMed]

29. Cohn JD, Johnson G, Ziesche S, et al. A comparison of enalapril with hydralazine-isosorbide dinitrate in the treatment of chronic congestive heart failure. N Engl J Med. 1991;325:303–310.[PubMed]

30. Rich MW, Vinson JM, Sperry JC, et al. Prevention of readmission in elderly patients with congestive heart failure: results of a prospective randomized pilot study. J Gen Int Med. 1993;8:585–590.[PubMed]

31. Monane M, Bohn R, Gurwitz JH, Glynn RJ. Noncompliance with congestive heart failure therapy in the elderly. Arch Int Med. 1994;154:433–437.[PubMed]

32. Packer M, O’Connor CM, Ghali JK, et al. Effect of amlodipine on morbidity and mortality in severe chronic heart failure. N Engl J Med. 1996;335:1107–1114.[PubMed]

33. The Multicenter Diltiazem Postinfarction Trial Research Group. The effect of diltiazem on mortality and re-infarction after myocardial infarction. N Engl J Med. 1988;319:385–395.[PubMed]

34. Cohn JN. Physiological rationale for co-treatment with diuretics in heart failure. Br Heart J. 1994;72(suppl 2):s63–s67.[PMC free article][PubMed]

35. Channer KS, McLean KA, Lawson-Matthew P, Richardson M. Combination diuretic therapy in severe heart failure a randomized controlled trial. Br Heart J. 1994;71:146–150.[PMC free article][PubMed]

36. Dormans TP, et al. Diuretic efficacy of high dose furosemide in severe heart failure: bolus injection versus continuous infusion. J Am Coll Cardiol. 1996;28:376–382.[PubMed]

37. Vargo DL, Brater DC, Rudy DW, Swan SK. Dopamine does not enhance furosemide induced natriuresis in patients with congestive heart failure. J Am Soc Neph. 1996;7:1032–1037.[PubMed]

38. Van veldhuisen DJ, Man Int Veld AJ, Dunselman PHJM, et al. Double blind placebo controlled study of ibopamine and digoxin in patients with mild to moderate heart failure: results of the Dutch Ibopamine multicenter study (DIMT) J Am Coll Cardiol. 1993;22:1564–1573.[PubMed]

39. Struthers AD. Aldosterone escape during ACE inhibitor therapy in chronic heart failure. Eur Heart J. 1995;16:103–106.[PubMed]

40. Packer M, Lee WH, Medina N, Yushak M, Kessler PD. Functional renal insufficiency during long term therapy with captopril and enalapril in severe chronic heart failure. Ann Int Med. 1987;106:346–354.[PubMed]

41. Gottlieb SS, Robinson S, Weir MR, Fisher ML, Krichen CM. Determinants of the renal response to ACE inhibition in patients with congestive heart failure. Am Heart J. 1992;124:131–136.[PubMed]

42. Packer M. The neurohormonal hypothesis: a theory to explain the mechanisms of disease progression in heart failure. J Am Coll Cardiol. 1992;20:248–254.[PubMed]

43. Azizi M, Chatellier G, Guyene TT, Murieta-Geoffrey D, Menard J. Additive effects of combined angiotensin converting enzyme inhibition and angiotensin II antagonism on blood pressure and renin release in sodium depleted normotensives. Circulation. 1995;92:825–834.[PubMed]

44. MacFadyen RJ, Barr CS, Struthers AD. Aldosterone blockade reduces vascular collagen turnover, improves heart rate variability and reduces early morning rise in heart rate in heart failure patients. Cardiovasc Res. 1997;35:30–34.[PubMed]

45. Pitt B. ACE inhibitor co-therapy in patients with heart failure: rationale for the randomized aldactone evaluation study (RALES) Eur Heart J. 1995;16:107–110.[PubMed]

46. Uretsky BF, Young JB, Shahidi FE, Yellen LG, Harrison MC, Jolly MK. Randomized study assessing the effect of digoxin withdrawal in patients with mild to moderate chronic congestive heart failure: Results of the PROVED trial. J Am Coll Cardiol. 1993;22:955–962.[PubMed]

47. The Digitalis Investigation Group. The effect of diogoxin on mortality and morbidity in patients with heart failure. N Engl J Med. 1997;336:525–533.[PubMed]

48. Packer M, Colucci WS, Sackner-Bernstein JD for the PRECISE Study Group. Double blind placebo controlled study of the effects of carvedilol in patients with moderate to severe heart failure—The PRECISE Trial. Circulation. 1996;94:2793–2799.[PubMed]

49. Waagstein F, Bristow MR, Swedberg K for the Metoprolol in Dilated Cardiomyopathy Trial Study Group. Beneficial effects of metoprolol in idiopathic dilated cardiomyopathy. Lancet. 1993;342:1441–1446.[PubMed]

50. Vantrimpoint P, Rouleau JL, Wun CC, et al. Additive beneficial effects of beta blockers to angiotensin converting enzyme inhibitors in the survival and ventricular enlargement (SAVE) study. J Am Coll Cardiol. 1997;29:229–236.[PubMed]

51. Gilbert EM, Abraham WT, Olsen S, et al. Comparative hemodynamic, LV functional and anti-adrenergic effects of chronic treatment with metoprolol vs carvedilol in the failing heart. Circulation. 1996;94:2817–2825.[PubMed]

52. Doughty RN, Sharpe N. Beta adrenergic blocking agents in the treatment of congestive heart failure: mechanisms and clinical results. Ann Rev Med. 1997;48:103–114.[PubMed]

53. Eichorn EJ, Bristow MP. Practical guidelines for initiation of beta adrenergic blockade in patients with chronic heart failure. Am J Cardiol. 1997;79:794–798.[PubMed]

54. Hall SA, Cigarroa CG, Marcoux L, Risser RC, Grayburn PA, Eichorn EJ. Time course of improvement in left ventricular function, mass, and geometry in patients with congestive heart failure treated with beta adrenergic blockade. J Am Coll Cardiol. 1995;25:1154–1161.[PubMed]

55. Stevenson LW, Dracup KA, Tillisch JH. Efficacy of medical therapy tailored for severe congestive heart failure in patients transferred for urgent cardiac transplantation. Am J Cardiol. 1989;63:461–464.[PubMed]

56. The Cardiac Arrhythmia Suppression Trial II Investigators. Effect of the antiarrhythmic agent moricizine on survival after myocardial infarction. N Engl J Med. 1992;327:227–233.[PubMed]

57. Doval HC, Nul DR, Grancelli HO, Perrone SV, Bortman GR, Curiel R. Randomized trial of low dose amiodarone in severe congestive heart failure. Lancet. 1994;344:493–498.[PubMed]

58. Singh SN, Fletcher RD, Fisher SG for the CHF STAT Investigators. Amiodarone in patients with congestive heart failure and asymptomatic ventricular arrhythmia. N Engl J Med. 1995;333:77–82.[PubMed]

59. Stevenson WG, Ridker PM. Should survivors of myocardial infarction with low ejection fraction be routinely referred to arrhythmia specialists. J Am Med Ass. 1996;276:481–485.[PubMed]

60. Doval HC, Nul DR, Grancelli HO, et al. Nonsustained ventricular tachycardia in severe heart failure—independent marker of increased mortality due to sudden death. Circulation. 1996;94:3198–3203.[PubMed]

61. AVID Trial Executive Committee. Are implantable cardioverter-defribillators or drugs more effective in prolonging life. Am J Cardiol. 1997;79:661–663.[PubMed]

62. Curfman GD. Inotropic therapy for heart failure—an unfulfilled promise. N Engl J Med. 1991;325:1509–1510.[PubMed]

63. Dies F, Krell MJ, Whitlow P, et al. Intermittent dobutamine in ambulatory outpatients with chronic cardiac failure. Circulation. 1986;74:38.

64. Packer M, Carver JR, Rodeheffer RJ for the PROMISE Study Research Group. Effect of oral milrinone in severe chronic heart failure. N Engl J Med. 1991;325:1468–1475.[PubMed]

65. Poole Wilson PA. Heart failure. Unfinished business—a possible role for vasodilators. Int J Cardiol. 1993;40:1–6.[PubMed]

66. Adamopoulos S, Piepoli M, Qiang F, et al. Effects of pulsed beta stimulant therapy on beta receptors and chronotropic responsiveness in chronic heart failure. Lancet. 1995;345:344–349.[PubMed]

67. Hunn D, Pedersen WR, Beccker R, et al. Benefits of attending a heart failure clinic. Circulation. 1990;82:609.

68. West JA, Miller NH, Parker KM, et al. A comprehensive management system for heart failure improves clinical outcomes and reduces medical resource utilization. Am J Cardiol. 1997;79:58–63.[PubMed]

69. McKelvie RS, Teo KK, McCartney N, Humen D, Montague T, Yusuf S. Effects of exercise training in patients with congestive heart failure: a critical review. J Am Coll Cardiol. 1995;25:789–796.[PubMed]

70. Jenkinson C, Jenkinson D, Shepperd S, Layte R, Petersen S. Evaluation of treatment for congestive heart failure in patients aged 60 years and older using generic measures of health status (SF36 and COOP charts) Age and Ageing. 1997;26:7–13.[PubMed]

71. Myers J, Gullestad L, Vagelos R, Bellin D, Do D, Ross H, Fowler M. Clinical, hemodynamic and cardipulmonary exercise test predictors of outcome in patients referred for heart failure evaluation. J Am Coll Cardiol. 1997;29:98–160.

72. Chomsky Lang CC, Rayos GH, Shyr Y, et al. Hemodynamic exercise testing—a valuable tool in the selection of cardiac transplantation candidates. Circulation. 1996;94:3176–3183.[PubMed]

Use this case study as an educational tool by answering the questions posed by the author, then reviewing the answers further down.

At 6:45 a.m., your unit is dispatched for a 50-year-old male with chest pain. You and your partner proceed to the scene, with a response time of approximately eight minutes. The closest hospital from the scene is 40 miles away.

You arrive at the scene, don appropriate BSI precautions and ensure that the area is safe, then knock on the door of the patient's residence. A middle-aged male answers the door and identifies himself as the patient. You note that he is diaphoretic and anxious, and is clenching his fist against the center of his chest.

1. What is the significance of the patients clenched fist in the center of his chest?

You sit the patient down and perform an initial assessment (Table I). Your partner attaches a pulse oximeter and prepares to administer oxygen to the patient.

Your partner administers 100% oxygen to the patient with a nonrebreathing mask while you perform a focused history and physical examination (Table II). The patient tells you that his doctor prescribed nitroglycerin for him; however, because he recently moved into the house, he thinks it's still packed in one of the boxes.

2. What are the physiologic effects of nitroglycerin?

After confirming no history of bleeding disorders or allergies, you administer 324 mg of aspirin to the patient. Your partner obtains baseline vital signs and a SAMPLE history (Table III). The patient remains conscious and alert, but is becoming increasingly restless. You attach the patient to a cardiac monitor and interpret his cardiac rhythm as sinus tachycardia at 110 beats per minute.

After administering 0.4 mg of nitroglycerin sublingually to the patient, you and your partner attach the remaining ECG leads and obtain a 12-lead tracing of the patient's cardiac rhythm. As your partner stands up to retrieve the stretcher from the ambulance, you tell him that it looks as though the patient may be having an anterior wall MI.

3. How could this patient's current blood pressure and heart rate affect his condition?

The patient's chest pressure is unrelieved following two more doses of sublingual nitroglycerin. You place him on the stretcher and load him into the ambulance. En route to the hospital, you continue oxygen therapy and successfully establish an IV of normal saline with an 18-gauge catheter. Reassessment of his blood pressure reveals a reading of 140/88 mmHg. Because three doses of nitroglycerin failed to relieve his pain, you administer 2 mg of morphine sulfate via IV push. Within 10 minutes, the patient tells you that the pressure in his chest has improved and is now a "3" on a 0--10 scale. With an estimated time of arrival at the ED of 20 minutes, you begin an IV infusion of nitroglycerin at 10 µg/min and perform an ongoing assessment (Table IV).

The patient's condition continues to improve en route to the hospital. You ask him if he has a history of ulcers, bleeding disorders, recent surgeries or stroke. He tells you that other than his high blood pressure and occasional chest pain, he has no other medical problems. You call your radio report to the receiving facility and continue to monitor the patient.

4. Why are you asking the patient these specific questions?

The patient tells you that he is still experiencing chest pressure; however, it is less severe. Since his blood pressure remains stable (130/84 mmHg), you administer another 2 mg dose of morphine via IV push. You continue to monitor the patient's vital signs and cardiac rhythm. Your estimated time of arrival at the hospital is 5--10 minutes.

5. Are there any special considerations for this patient?

Upon arriving at the emergency department, the patient states that he is pain-free. You give your verbal report and field-obtained 12-lead ECG to the attending physician. Following additional assessment in the emergency department, the patient is diagnosed with an acute anterior wall myocardial infarction. Following successful treatment with fibrinolytic therapy, he is admitted to the cardiac care unit and transferred to a cardiac rehabilitation facility 10 days later.

Cardiac Case Study: Answers and Summary

1. What is the clinical significance of the patient’s clenched fist in the center of his chest?

Ischemic cardiac chest pain is typically described as being crushing, tight, oppressive, pressuring or constricting in nature. Patients may describe their pain as though a vise were placed around their chest or the sensation that an elephant is sitting on their chest, while others may only report a vague or "strange" sensation in their chest. The pain associated with cardiac ischemia is usually substernal; however, it may be localized to the epigastrium and is commonly mistaken for indigestion.

A clenched fist in the center of the chest (the precordium) conveys the feeling of pressure or squeezing and is called Levine's sign (see the photo on page 50). The presence of Levine's sign is suggestive, but not conclusive, of cardiac-related chest pain and should increase your index of suspicion.

Chest pain or discomfort is the most common presenting symptom of an acute coronary syndrome (ACS), occurring in 70%--80% of patients. However, 20% or more of patients with acute myocardial infarction present with no pain or discomfort at all. Elderly patients and patients with diabetes may present without classic symptoms or with only vague, nonspecific symptoms, such as malaise, lightheadedness, syncope, changes in mentation or sudden diaphoresis.

Patients with cardiac ischemia may also present with referred pain to other areas of their body, such as the jaw, arm, shoulder or back. Less commonly, patients may present with atypical chest pain, which may be described as sharp or stabbing in nature.

During your general impression of the patient with chest pain or pressure, look for clues suggestive of cardiac compromise, such as diaphoresis, restlessness or apprehension. The absence of chest pain or the presence of atypical chest pain, however, does not rule out an ACS--especially if the patient has other signs and symptoms and a history of cardiac disease (e.g., prescribed nitroglycerin).

Acute coronary syndrome is a term used to describe many types of compromised circulation to the heart muscle, including unstable angina pectoris or acute myocardial infarction. Because the clinical presentations of the two are extremely similar, if not identical (i.e., unrelieved chest pain, ECG changes, diaphoresis), treatment should focus on the assumption that acute myocardial infarction is occurring.

2. What are the physiologic effects of nitroglycerin?

Before discussing the physiologic effects of nitroglycerin, a brief review of coronary atherosclerosis, myocardial ischemia and angina pectoris is in order.

Coronary atherosclerosis is a progressive disease characterized by the buildup of lipid-laden plaque within the lumen (channel) of the coronary artery. Atherosclerosis causes narrowing of the artery (decreasing coronary blood flow) and hardening of the artery (limiting the ability of the artery to dilate). These negative consequences of atherosclerosis reduce the ability of the heart to accommodate increases in myocardial oxygen demand, such as that caused by stress or exertion.

When the scale of myocardial oxygen supply and demand is unbalanced, the patient develops ischemic chest pain or pressure (angina pectoris). Ischemia, which is defined as a relative deprivation of oxygen, occurs when oxygen demand exceeds supply, and is a reversible condition with prompt treatment.

Angina is described as being stable or unstable. Stable angina is characterized by a relatively predictable sequence of events. Patients are often aware of the extent of exertion that precipitates their chest pain (e.g., walking one block); therefore, they limit their activities in order to avoid symptoms. Additionally, patients are also aware of what they need to do to resolve their symptoms (e.g., a specific period of rest, nitroglycerin). Following resolution of their chest discomfort, many patients with stable angina never call EMS.

Unstable angina occurs when the patient experiences a change in his typical anginal pattern, indicating advanced coronary atherosclerosis and an oxygen supply-demand mismatch that is not so easily balanced with rest and nitroglycerin. Relative to stable angina, the patient with unstable angina experiences "off-pattern" chest pain, such as when exertion is minimal or when myocardial oxygen demand is otherwise low (e.g., during sleep). Additionally, the usual treatment modalities of rest and/or nitroglycerin afford them minimal or no relief from their symptoms. This change may prompt a call to EMS.

Nitroglycerin (NTG) causes relaxation of vascular smooth muscle (vasodilation), promoting systemic pooling of venous blood. This decreases the volume of blood that is returned to the heart (preload), as well as the amount of resistance that the heart must pump against (afterload). The combined effects of decreased preload and afterload cause an overall decrease in myocardial oxygen demand and consumption.

Additionally, nitroglycerin may dilate the coronary arteries and promote collateral circulation, thus improving oxygen supply to the ischemic myocardium. Collateral circulation, also referred to as "arteriogenesis," is a process in which smaller arteries that are normally closed become patent (open up) and connect two larger arteries or different parts of the same artery. Over time, myocardial ischemia can promote collateral vessels to grow, forming a "detour" for blood flow around the blocked coronary artery.

Because nitroglycerin dilates the systemic blood vessels, it can result in hypotension. Therefore, its use is generally contraindicated in patients with a systolic BP of less than 90 mmHg, as well as in patients who have taken Viagra (sildenafil), Levitra (vardenafil) or Cialis (tadalafil) within the past 24--36 hours. These drugs, which are used to treat sexual dysfunction, also cause vasodilation and, when used concomitantly with nitroglycerin, can result in potentially life-threatening hypotension. EMS providers should follow local protocol or contact medical control as needed regarding the use of nitroglycerin.

3. How could this patient's current blood pressure and heart rate affect his condition?

This patient's history, physical examination and 12--lead ECG findings suggest acute myocardial infarction (AMI) involving the anterior (front) wall. The patient's hyperdynamic vital signs--hypertension and tachycardia--indicate a discharge of epinephrine and norepinephrine from the sympathetic nervous system, most likely caused by a combination of pain, anxiety/fear and myocardial ischemia and injury. Epinephrine increases the rate (chronotropy) and strength (inotropy) of cardiac contractions and norepinephrine increases systemic blood pressure by constricting the blood vessels.

This patient's vital signs represent a classic case of "more is not better!" In order for the heart to beat stronger and faster, it requires and uses more oxygen. Additionally, an elevated blood pressure increases afterload (ventricular resistance), further increasing myocardial oxygen demand.

Unfortunately, in this patient, an occluded coronary artery is blocking the flow of oxygenated blood to the area of the myocardium that needs it most--the injured area. This increase in myocardial oxygen demand and consumption and decrease in myocardial oxygen supply can enlarge the area of injury, resulting in greater myocardial damage.

The anterior wall is the largest part of the heart and tends to sustain significant damage as the result of an MI. As the area of injury increases, lethal cardiac dysrhythmias, such as ventricular fibrillation (v--fib) or ventricular tachycardia (v--tach), can occur. Additionally, if an extensive area of the anterior wall is damaged, the patient can develop acute CHF and, in more severe cases, cardiogenic shock. Cardiogenic shock, which has a very high mortality rate, occurs when the heart is severely damaged and is no longer able to adequately perfuse the body.

4. Why are you asking the patient these specific questions?

This patient is a potential candidate for fibrinolytic (clot-buster) therapy; therefore, you should conduct a field screening to determine if he is eligible for this treatment. Although fibrinolytic therapy is not commonly initiated in the prehospital setting, the information you obtain regarding the patient's eligibility or ineligibility, in addition to the 12-lead ECG obtained in the field, will be valuable to the physician and can decrease the "door-to-drug" time when the patient arrives in the emergency department.

Fibrinolytic agents (Table V) work by a chemical process that converts plasminogen to plasmin, the central enzyme of the physiologic plasminogen system. Plasmin in turn digests fibrin, the active component of the clot matrix, through a process called fibrino­lysis. Fibrinolysis dissolves the clot that is occluding the coronary artery, thus reestablishing distal perfusion. The goal of fibrinolytic therapy is to halt the infarction process and salvage areas of ischemic and injured myocardium.

The indications or inclusion criteria for fibrinolytic therapy are summarized in Table VI. Although EMT-Basics and EMT-Intermediates are not usually trained to interpret ECG rhythms, they can, through index of suspicion based on the patient's signs and symptoms, suspect AMI and conduct a field screening, especially if the time of onset is less than 12 hours.

Because of the interaction of fibrinolytics with the body's hematologic system, strict criteria must be met before the patient can be eligible for fibrinolytic therapy. If given to the wrong patient, fibrinolytics can cause life-threatening hemorrhage. Table VII summarizes the absolute and relative contraindications or exclusion criteria for fibrinolytic therapy. Some patients with certain relative contraindications may still be eligible for fibrinolytic therapy, based on a careful evaluation by the physician.

5. Are there any special considerations for this patient?

There are several issues to consider when treating and monitoring this patient. As previously discussed, nitroglycerin (being administered to this patient via continuous IV infusion) can cause hypotension. Therefore, careful monitoring of the patient's blood pressure is essential. Hypotension in a patient with a sick heart can have disastrous consequences.

You have also administered a total of 4 mg of morphine to the patient. Morphine, a narcotic analgesic, can depress the central nervous system, resulting in a decreased level of consciousness, hypoventilation, bradycardia and hypotension. While most people will not experience significant CNS depression with low doses of morphine, you should have a BVM handy to assist ventilations, as well as naloxone (Narcan) to reverse the effects of the morphine. Narcan competitively binds with opiate receptor sites in the body and reverses the CNS depression associated with narcotic administration.

Continuous cardiac monitoring is an essential part of cardiac patient management, especially in this patient, whose 12-lead ECG indicates that an MI is in progress. You must be alert for the development of warning signs of a potentially lethal dysrhythmia, such as premature ventricular complexes (PVCs). You should also observe the patient for any sudden changes in his heart rate. Anterior wall MIs can result in significant tachycardia or bradycardia, both of which can further complicate the clinical picture.

When caring for a potentially unstable cardiac patient, especially when your transport time is lengthy, you must remain cognizant of the fact that because you are alone in the back with the patient, your capabilities are limited to defibrillation and one-person CPR if the patient develops cardiac arrest. Therefore, it would be prudent to request additional assistance or arrange to rendezvous with another EMT or paramedic while en route to the hospital.


This case study represented a patient with a relatively uncomplicated myocardial infarction that, after prompt prehospital care and transport, was successfully halted in the emergency department with fibrinolytic therapy.

This patient was provided excellent care in the prehospital setting because the paramedic and his EMT-B partner worked together effectively as a team. Although ECG monitoring, IV therapy and medication administration are beyond the usual scope of practice of an EMT-B, many EMS systems are training their EMT-Bs to assist with these important procedures and interventions. This involves preparing IV equipment and supplies, applying the cardiac monitor, and recognizing and handling the various paramedic medications. This enhanced role of the EMT-B allows the paramedic to perform a more focused and careful patient assessment.

A cohesive working relationship between BLS and ALS personnel is absolutely crucial to the outcome of the patient. Although each level of prehospital provider possesses a different knowledge of pathophysiology and patient management, it is the combined contributions and efforts of each provider that will afford patients the high quality of care they deserve.


  • ACLS for EMT-Basics. Jones and Bartlett, Publishers/AAOS, 2003.
  • Advanced Cardiac Life Support: Principles and Practice. American Heart Association, 2003.
  • Emergency Care and Transportation of the Sick and Injured, 8th Edition. Jones and Bartlett, Publishers/AAOS, 2002.
  • Prehospital Advanced Cardiac Life Support, 2nd Edition. Brady Publishing, 2004.

0 thoughts on “Cardiac Case Study Nursing Students”


Leave a Comment

Your email address will not be published. Required fields are marked *