Objectives

1. Describe the various diagnostic tests used in cardiovascular disease ( EKG, Stress test, Phonocardiogram, Echocardiogram, various types of cardiac catheterization). For each test, be able to give a brief description of the procedure used and major uses of the test (i.e. the type of information provided by the test and/or the abnormalities it would be used to diagnose).

2. Identify the factors (modifiable and non-modifiable) that increase the likelihood of developing coronary atherosclerotic disease. (pp. 454-455)

3. Differentiate between myocardial ischemia and myocardial infarction, including the signs and symptoms of each. (pp. 461-464)

4. Identify the most common sites of coronary atherosclerotic lesions. (p. 454)

5. Identify the characteristic diagnostic triad associated with a myocardial infarction. (p. 464-465)

6. Know all underlined terms and * questions, including * case study questions.

Be sure to study the information in the manilla folders for each technique.

Electrocardiogram (EKG) (pp. 434-437)

An EKG is a graphic recording of the heart's electrical activity - it follows the propagation of an electrical impulse throughout the heart. Study the diagram of a single EKG recording on p. 434 of your text.

* Describe the cardiac electrical events which correspond to each of the following : P wave, PR interval, QRS complex, ST segment and T wave. Label each of these on the EKG below.

* What types (name 4) of heart problems can be diagnosed using an EKG?

* What changes on EKG are often found with each of the following : myocardial ischemia, myocardial infarction, ventricular hypertrophy, atrial hypertrophy. (p. 435-439, Figs. 31-9, 31-15)

* What do you think are some of the advantages of this technique?

Compare some of the abnormal EKG recordings in the folder with the normal recordings in your text. Look for any differences. You will not be expected to identify any specific abnormalities on the EKG examples.

Exercise Stress Test, (p. 441)

In this procedure, a patient's EKG is recorded while s/he is undergoing increasingly difficult exercise levels (such as increasing the speed and/or incline of a treadmill). This procedure is important in detecting myocardial ischemia.

* Why would this technique (increasing exercise levels) be likely to induce myocardial ischemia? (pp. 452-453)

* What change(s) would you expect to see on an EKG with myocardial ischemia? (pp. 434-435, Fig. 31-9, p. 462)

* What is the classic symptom a patient with myocardial ischemia experiences? (p. 462)

Phonocardiogram

A phonocardiogram is a permanent graphic recording of the sounds made during the cardiac cycle. A microphone positioned on the chest wall receives sound waves which are amplified and recorded.

* What is another, simpler, method a physician can use to study a patient's heart sounds?

A phonocardiogram is usually recorded in conjunction with an EKG and sometimes a carotid pulse. Study the example below and those in the folder.

* To what do the first heart sound (S1) and the second heart sound (S2) correspond? (p. 433)

* What is occurring in the heart during the following intervals :

between S1 and S2

between S2 and S1 (of the next cardiac cycle)

* What types of cardiac problems would be detected by this technique? (pp. 433-434)

Echocardiogram (pp. 437-439, Fig. 30-9, 30-11, 30-12)

In an echocardiogram, a transducer emitting ultrasound (high frequency) waves is placed on the patient's chest. The ultrasound waves bounce off various heart structures (such as valve leaflets and chamber walls) and are received by the transducer.

* What types of heart abnormalities (name 3) are often detected with this technique?

Study the 1D and 2D echocardiograms found in the manilla folder.

Cardiac catheterization (pp. 442-449)

This technique involves the insertion of catheters into the cardiovascular system. There are a number of variations on this technique and various types of information can be gained (p. 443). In addition, some catheterization techniques are used for treatment of cardiovascular problems.

* Describe the differences between right-sided and left-sided approaches used in cardiac catheterization. (pp. 443-444)

* What is meant by coronary angiography? What information could be gained by this procedure? Would a right-sided or left-sided approach be used in this technique? (pp. 443-444)

Examine the Swan-Ganz catheter. (Figs. 30-20 and 30-21)

* What type of measurements are taken with this catheter? (p. 446)

* For what heart conditions (name 3) would this catheter be used? (pp. 447-448)

A variety of pulse generators can be used for pacing therapy, to regulate the heart rate (see p. 476). Among these are the pacing catheter (see example in lab) which is used temporarily, for instance if a heart stops beating during open heart surgery. For permanent management of dysrhythmias, a cardiac pacemaker can be implanted. Examine the various pacemakers and the radiograph of an implanted pacemaker out in lab.

Another technique involving catheter use is angioplasty.

* What is meant by angioplasty? Describe this technique and the conditions it is used to treat. (pp. 473-474)

What potential problems or complications may occur with any type of catheterization?

Atherosclerosis of Coronary Artery  (PH 804, 813, 814) (Fig 7-11 and 7-12, pp. 104-105) Click here

First observe a slide of an early atherosclerotic lesion (PH 813). The pink, noncellular material in the intima of the coronary artery is the atherosclerotic plaque. This lesion has already reduced the lumen by about 20%. Now observe one of the later atherosclerotic plaques (PH 804 or PH 814). Note the degree of occlusion by the lesion. It may take years for plaque to reach this size.

          1. Normal coronary artery, microscopic *
          2. Mild coronary atherosclerosis, microscopic *
          3. Severe calcific coronary atherosclerosis, microscopic *
          4. Coronary atherosclerosis, cross sections, gross
          9. Coronary thrombosis, gross
          10. Coronary thrombosis, gross
          11. Coronary thrombosis, microscopic *
          Left anterior descending coronary artery, advanced atherosclerosis, gross.

* Clinically significant lesions (which produce myocardial ischemia) usually obstruct over percent of the vessel lumen. (p. 454)

Do you think any of these lesions would be clinically significant? Which ones?

Normal, Healthy and Atherosclerotic Aortas (pp. 103-107, Fig. 31-3, 453-454)

Notice the opened aorta from a 27 year old male. Although it has a smooth inner lining, it shows the beginning of atherosclerosis as thin wavy yellow streaks of fat. The regular holes along the aorta are lumbar artery branchings.

        16. Aorta, lipid streaks, gross
        17. Aorta, lipid streaks, gross
 

Now observe the aorta from a 77 year old man. Its lining is rough with large areas replaced with fatty, lumpy plaques. Feel the lumps, noticing that some are hard from calcium deposits.

Can you picture how blood would flow over this aorta's lining compared to normal?

        18. Aortas with mild, moderate, and severe atherosclerosis, gross *
        19. Aorta, atheromatous plaque, medium power microscopic *
        20. Aorta, atheromatous plaque, high power microscopic *
        21. Aorta, atheromatous plaque, high power microscopic *
        Aortic atherosclerosis demonstrated in three aortas, gross.

* How would this rough lining affect blood?

Any artery in the body having atherosclerosis would have a similar structure.

Heart with Coronary Atherosclerosis (Fig. 31-3, 453-454, 461-468, 103-107)

Notice the excessive amount of pericardial fat present on this heart. Also note the presence of atherosclerotic plaques in some of the coronary arteries (which have been opened).

        1. Normal coronary artery, microscopic *
        2. Mild coronary atherosclerosis, microscopic *
        3. Severe calcific coronary atherosclerosis, microscopic *
        4. Coronary atherosclerosis, cross sections, gross
        9. Coronary thrombosis, gross
        10. Coronary thrombosis, gross
        11. Coronary thrombosis, microscopic *
        Left anterior descending coronary artery, advanced atherosclerosis, gross.

* What potential complications could occur as a result of these plaques? (pp. 104-105)

Hemorrhagic Coronary Infarction (pp. 106-107, 453, 463, Fig. 31-12)

This is a sagittal section through the interventricular septum. It is from a patient who died of a myocardial infarction severe enough to cause rupturing of the coronary vessels. Notice the dark hemorrhaged blood.

        Interventricular septum, recent myocardial infarction, gross.

* What does "myocardial infarction" mean? (p. 453)

Arteriosclerosis of Coronary Artery with Thrombus (pp. Fig. 7-12, pp. 461-465)

Distinguish between arteriosclerosis and atherosclerosis. (p. 103)

Note, on the wall chart, the obstruction in the coronary artery cross-section.

       1. Normal coronary artery, microscopic *
       9. Coronary thrombosis, gross
       10. Coronary thrombosis, gross
       11. Coronary thrombosis, microscopic *

Acute Myocardial Infarction (Heart Attack) (pp. 106-107, 461-465)

A heart attack is typically produced by the sudden plugging of one of the coronary arteries, resulting in myocardial ischemia lasting over 30 to 45 minutes, producing irreversible cellular damage and death.

       14. Remote myocardial infarction, gross
       Interventricular septum, recent myocardial infarction, gross.

* What portion of this heart has sustained myocardial infarction? Is this the most common site?

* What is the difference between a transmural and a subendocardial infarction? (Fig. 31-12, p. 463).

Describe the tissue changes which occur within the first 24 hours after acute MI. (p. 464)

* Describe 5 factors which influence the degree of functional impairment following an MI. (p. 464)

Complications of Acute Myocardial Infarction (pp. 466-468)

Locate each of the following pathological complications of an MI on the wall chart : Thrombus (blood clot) in Left Atrium, Thrombus in Right Ventricle, Rupture of Ventricle in MI, Rupture of Ventricular Septum in MI, Pericarditis.

* What causes thrombus formation after acute MI? (p. 467)

* What does embolization mean? (pp. 102, 468)

* Should a thrombus located in the right ventricle dislodge and move, where would it go?

       27. GIF animation of pulmonary thromboembolus, diagram
       69. Lung, pulmonary thromboembolus, gross
       70. Lung, pulmonary thromboembolus, gross
       73. Lung, pulmonary thromboembolus, gross
       74. Lung, pulmonary thromboembolus, low power microscopic*

* What would be the consequences of rupture of the ventricular septum? (p. 467)

       Interventricular septum, recent myocardial infarction, gross.

* Cardiac tamponade is associated with what complication of acute MI? (p. 467)

       15. Left ventricular aneurysm, gross

Case Study 1 - Acute Myocardial Infarction

George M., a 54 year-old executive, was rushed to the hospital after experiencing substernal pain radiating down his arms and into his neck. He also experienced dizziness, nausea, diaphoresis and shortness of breath.

His history revealed some episodes of substernal chest discomfort with exertion, hypertension, obesity and smoking. His father and brother died at early ages of myocardial infarction. Recently, Mr. M. had been under some degree of tension due to business reverses and problems with his two teenage children.

Physical examination revealed a blood pressure of 190/100 mmHg, pulse 130 and irregular, temperature 38 C. Chest examination revealed fine inspiratory rales in both lung bases. Chest X-ray showed cardiomegaly and pulmonary congestion. EKG revealed a sinus tachycardia with frequent premature ventricular contraction. Laboratory studies showed elevations in cholesterol, uric acid, CPK, LDH and SGOT enzymes. A diagnosis of acute anterior wall infarction was made.

1. What risk factors may have contributed to George's development of acute MI? (pp. 454-455)

*2. Did George have angina? Is anginal pain different from the pain of a heart attack? If so, how? (pp. 462, 464)

*3. What relationship, if any, did George's history of hypertension have to his subsequent MI? (p. 457)

4. What coronary artery is obstructed when the client is termed to have an "anterior wall infarction"? What portion of the heart musculature is involved? (p. 463, Figs. 31-11, 31-13)

5. What might be the reason(s) for George's tachycardia? What is causing his premature ventricular contractions? Do PVCs affect the pulse? (pp. 468-469)

*6. Is there any relationship between the following diagnostic findings: inspiratory rales, cardiomegaly and pulmonary congestion? If so, relate them to acute MI? (p. 466)

*7. Why are George's enzymes elevated? (p. 465)

*8. What are the major complications George may develop following his MI? (pp. 466-468, pp. 19-22 in this booklet)

9. What principles of therapy will probably be employed to treat George over the next 3-5 days. (pp. 471-475)

10. How will George's infarction heal? What is his long-range outlook? (p. 464)

Case Study 2 - Congestive Heart Disease

Lettie F., a 65 year-old widow, had been experiencing increasing dyspnea on exertion, orthopnea and paroxysmal nocturnal dyspnea (PND). In addition, her ankles remained swollen, her appetite was decreased, and she complained to her physician she felt "weak and tired" most of the time.

Physical examination revealed an obese woman with bilateral pitting edema of the ankles, abdominal distension, shortness of breath on mild exertion and hypertension. The apical impulse was forceful and displaced to the left at the sixth intercostal space. EKG revealed chronic myocardial ischemia. Chest X-ray demonstrated cardiomegaly and pulmonary venous congestion.

A diagnosis of chronic congestive heart disease was made.

     dilation
          Normal cardiac muscle, medium power microscopic *
          Heart, dilated cardiomyopathy, gross [XRAY]
          Heart, dilated cardiomyopathy, gross
      hypertrophy
          5. Hypertrophy, heart, gross
          Heart, hypertension with left ventricular hypertrophy, gross
          Heart, cardiomyopathy, microscopic *

*1. Compare the symptoms associated with right-sided heart failure to those of left-sided heart failure. Which does Lettie show symptoms of? (pp. 466, 498-500)

*2. What relationship does Lettie's long-term hypertension and obesity have to her diagnosis of chronic congestive heart disease? (pp. 457-459)

*3. Define orthopnea and paroxysmal nocturnal dyspnea. (pp. 429, 498-499)

*4. Describe how the EKG and chest X-ray confirm the diagnosis of congestive heart disease. (pp. 435, 441)

5. What medical therapies will probably be used to improve Lettie's heart function? (pp. 471-472)

8Copyright 2001 - Augustine G. DiGiovanna - All rights reserved.