Question

Samantha, a 74-year-old woman with a history of rheumatic fever while in her twenties, presented to her physician with complaints of increasing shortness of breath ("dyspnea") upon exertion. She also noted that the typical swelling she's had in her ankles for years has started to get worse over the past two months, making it especially difficult to get her shoes on toward the end of the day. In the past week, she's had a decreased appetite, some nausea and vomiting, and tenderness in the right upper quadrant of the abdomen.On physical examination, Samantha's jugular veins were noticeably distended. Auscultation of the heart revealed a low-pitched, rumbling systolic murmur, heard best over the left upper sternal border. In addition, she had an extra, "S3" heart sound. A chest X-ray reveals a normal cardiac silhouette that is normal in diameter, but her physical examination reveals hepatomegaly and ascites, as well as pitting edema in her ankles. She is advised to wear support stockings and given a prescription for digoxin. Two weeks later she returns to the office for a follow-up visit; upon physical examination, she still has significant hepatomegaly and pitting edema, and is significantly hypertensive (i.e. she has high blood pressure). Her physician prescribes a diuretic called furosemide (or "Lasix").

1. What is causing the low-pitched, rumbling murmur (both in general and specific anatomical and physiological terms)? Why is it heard best over the left upper sternal border? Which valve is involved?

2. What is causing the "S3" heart sound? What portion of the cardiac cycle will it be heard in and why?

3. Is Samantha's history of rheumatic fever relevant to the current symptoms? Why or why not? What causes rheumatic fever and what might it cause in Samantha years after her infection? Why is the diagnosis of the specific valve involved in the systolic murmur important?

4. Does the normal diameter of the heart on X-ray rule out a possible cardiac diagnosis? What is meant by the term “concentric hypertrophy” and why might it be happening in Samantha’s heart?

5. What is meant by the terms “hepatomegaly” and “ascites” and why are they happening? Why are her jugular veins distended? Be specific in terms of blood pressure and Starling forces.

6. What is pitting edema and what is causing it?

7. Why is she advised to wear support stockings? If she had atherosclerosis or blockage of a femoral artery, would this be an advisable diagnosis? Why or why not?

8. Is the stress being placed on Samantha’s heart pre-load or after-load and why?

9. What is the general diagnosis for Samantha’s condition? What would the diagnosis be if there were pulmonary edema instead of systemic edema?

10. Why is Samantha started on digoxin? How does it work? State your answers in terms of chronotropism and inotropism, the Na+/K+ ATPase, cytoplasmic Ca++ concentrations, and the proteins in a cardiomyocyte’s sarcomere.

11. What happened to Samantha in the two weeks before her follow-up visit? In other words, how did her body begin to compensate for decreased stroke volume? Utilize cardiac output, sympathetic nervous system, vasoconstriction to “less vital” organs (including the kidney) the renin-angiotensin-aldosterone (R-A-A) axis, Angiotensin II, ADH, pre-load and after-load, the Frank-Starling law, and the actions of digoxin.

12. Why was she given Lasix medication, and how does it work?

Answer 1

1. What is causing the low-pitched, rumbling murmur (both in general and specific anatomical and physiological terms)? Why is it heard best over the left upper sternal border? Which valve is involved?

Mitral Stenosis or Diastolic Murmur. It is heard best over upper part because of the friction of mitral valve over thickened septal wall during systole. Any maneuver which decreasing preload or afterload such as Valsalva or abrupt standing makes it even more louder.

2. What is causing the "S3" heart sound? What portion of the cardiac cycle will it be heard in and why?

S3 is otherwise called as ventricular gallop followed by S2 when the mitral valve closes. It occurs during rapid filling and expansion of the ventricles. It occurs while tensing of the chordae tendineae during "ventricular filling phase". It is well heard with the bell-side of the stethoscope.

3. Is Samantha's history of rheumatic fever relevant to the current symptoms? Why or why not? What causes rheumatic fever and what might it cause in Samantha years after her infection? Why is the diagnosis of the specific valve involved in the systolic murmur important?

Yes. The current symptoms correlated with the rheumatic fever occurs in Samantha's early stage. Rheumatic fever can sometime cause damage to heart which can resume after 10 to 20 years of original illness. In severe cses, it damages the heart valves. It is caused by the pathogen called group A streptococcal bacteria commonly called as 'strep throat'. In most cases, strep throat is vanished with anitibiotics but few times it leads to secondary infetion causing thickening of the leaflets. It usually appears with the symptoms of fever, joint pains, rash and heart problems with symptoms of murmur due to thickened mitral valve. Most common diagnostic techniques are: cardiac MRI and cardiac CT.

4. Does the normal diameter of the heart on X-ray rule out a possible cardiac diagnosis? What is meant by the term “concentric hypertrophy” and why might it be happening in Samantha’s heart?

No. Normal diameter of the heart on X-ray rule cannot rule out the cardiac diagnosis. Concentratic hypertropy occurs without overall organ enlargement which is characterized by the hypertrophic growth of a hollow organ. This cannot be ruled out with overall heart diameter. In this case, the size of the heart muscle fibers are increased in size resulting in chamber enlargement. Samatha's heart is observed with mitral valve stenosis due to thickeing of mitral valve which obstruct the blood flow.