Congestive Heart Failure Case Study

Anatomy and Physiology Reviewhttp://www.nhlbi.nih.gov/health/health-topics/topics/hhw/printall-index.html

Background PathophysiologyWhat is heart disease?http://www.nhlbi.nih.gov/health/health-topics/topics/hdw/ What is heart failure?http://www.cvphysiology.com/Heart%20Failure/HF002.htm

About 5.8 million people in the United States have heart failure. The number of people who have this condition is growing.

Heart failure is more common in:

• People who are 65 years old or older. Aging can weaken the heart muscle. Older people also may have had diseases for many years that led to heart failure. Heart failure is a leading cause of hospital stays among people on Medicare.

• African Americans. African Americans are more likely to have heart failure than people of other races. They're also more likely to have symptoms at a younger age, have more hospital visits due to heart failure, and die from heart failure.

• People who are overweight or obese. Excess weight puts strain on the heart. Being overweight also increases your risk of heart disease and type 2 diabetes which increases your risk of heart failure.

• People who have had a heart attack.

• Men (Men have a higher rate of heart failure than women)

Clinical Significance:There are many major clinical concerns with CHF. The major ones are as follows:

Cardiovascular – increased pressure on the heart’s chambers causes fluid backup and a reduced forward flow of blood. The heart becomes unable to supply the body’s organ systems (including the cardiovascular system) with blood. This causes a decrease in cardiac output and BP, then causes vasoconstriction from the activation of the sympathetic nervous system.

Pulmonary – If the pressure from the left heart is significant enough to push blood the wrong direction, fluid will accumulate in the lungs. This can cause abnormal breath sounds, crackles in the lung, decreased oxygen and consequently shortness of breath.

Skin – due to decrease cardiac output and low oxygen saturation, skin may look pale, grey, or cyanotic. Fluid backup into the veins may cause swelling of the extremities and pitting of skin when pressed on.

GI – The fluid backup into the veins can cause an enlargement of the spleen and liver, as well as distension of the abdomen.

Neuro – Because of the decrease in cardiac output, the brain’s oxygen supply continues to decrease, causing things like confusion, weakness, dizziness, and

fatigue. Also, the decrease in blood pressure stimulates the sympathetic nervous system to attempt to raise cardiac output. (Cardiac output = HR + BP)

Diagnostic Strategies: History - the key elements of the history are to identify the following:

o In the case of acute heart failure, patients may have a fairly sudden onset shortness of breath, or difficulty breathing with lying down or with exercise.

o Rapid heartbeat or palpitations. o The patient may experience chest pain if the case of CHF is caused by a

heart attack.o Swelling in the lower extremitieso A history of hypertension, diabetes, obesity, heart valve malfunctions, and

previous heart disease all increase your chances for developing CHF. Physical exam-

o The patient may present with an irregular tachycardic pulse, distended neck veins and sometimes a third heart sound is noted.

o If the fluid has backed up into the lungs, shortness of breath, decreased breath sounds, lung crackles, and coughing may occur.

o Due to decreased oxygen sats, fingers and toes may appear slightly cyanotic.

o Enlargement of the liver and/or abdomeno Edema of the lower extremities and pitting when pressed upon

Labs – o EKG – can help show ischemia, MI, arrhythmias, and CAD that are

potential causes of heart failureo CBC, PT/PTT, BMPo Bun/Cr levels o ABG

Imaging – o A chest x-ray – can show fluid in lungs, increased heart size or other

abnormal findingso Echocardiogram – can show ventricular remodeling, dilation of the

chambers, or issues with the heart values that could cause CHF.

Case Study

Chief Complaint: 54-year-old woman with shortness of breath and swelling.

History: Martha Wilmington, a 54-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.

Family History: Mother was diagnosed with Hypothyroidism and Father was type II diabetic and passed away from a massive heart attack in 1991.

Social History: Former Smoker (2-pack a day); quit in 2009 but smoked for over 20 years. Does not drink alcohol.

Physical Examination: Martha'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. Pitting edema present in both feet/ankles. Patient is overweight/obese with a body weight of 225lbs and height of 5’2”. Overall all appearance of patient appears to be gray in color, with perfuse sweating and shortness of breath with fatigue brought on by activity. Both legs appear to be swollen with marked cyanosis presence in both feet. Rest does not relieve pain in legs, and periods of long sitting increase edema as noted by the patient.

Diagnostic Examination:Chest X-Ray SeriesEKGCBC with differentialBNP Blood Test or CRP TestThyroid Panel TestDoppler UltrasoundEchocardiographyStress TestHolter Monitor

Diagnosis: Left Sided Heart Failure

Differential Diagnosis: HypothyroidismRight Sided Heart Failure

Referral: CardiologistNutritionist/Trainer

Follow-up: 2 WeeksDiagnostic Results

Chest X-Rayhttp://www.radiologyassistant.nl/en/4c132f36513d4

BNP Blood Testhttp://www.chfpatients.com/tests/bnp.htm#bnp_levels http://www.heart-strong.com/files/heartstrong-BNParticleWebsite_1_.pdf

CRP Testhttp://my.clevelandclinic.org/heart/services/tests/labtests/crp.aspx

EKG

Patient Name: Martha Jones Age 54Sex: Female

BNP Levels 695 pg/mL

Doppler Ultrasound

Angiocardiography

Echocardiogramhttp://www.chfpatients.com/tests/echo.htm

Case Study Questions

1. What is causing this murmur?

2. What is causing her "S3" heart sound?

3. Is her history of rheumatic fever relevant to her current symptoms? Explain.4. A chest X-ray reveals a cardiac silhouette that is normal in diameter. Does this rule out a

possible problem with Martha's heart? Explain.

5. You examine Martha's abdomen and find that she has an enlarged liver ("hepatomegaly") and a moderate degree of ascites (water in the peritoneal cavity). Explain these findings.

6. Examination of her ankles reveals significant "pitting edema." Explain this finding.

7. She is advised to wear support stockings. Why would this help her?

8. Which term more accurately describes the stress placed upon Martha's heart -- increased pre-load or increased afterload?

9. What is the general term describing Martha's condition?

10. How might Martha's body compensate for the above condition?

11. Martha is started on a medication called digoxin. Why was she given this medication, and how does it work?

12. Two weeks after starting digoxin, Martha returns to the physician's office for a follow-up visit. On 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"). Why was she given this medication, and how does it work?

Answers:

1. A low-pitched, rumbling murmur is usually due to a stenotic (i.e. narrowed) valve. The left, upper sternal border is where the closing sound of the pulmonic valve is heard the best. Since Martha's murmur is heard best in this area, it is most likely due to pulmonic valve stenosis. Since the pulmonic valve leaflets are not fully opening, there is resistance to the forward flow of blood through this valve during ventricular systole. Thus, there is a harsh, low-pitched murmur of turbulent blood flow heard over the left, upper sternal border during ventricular systole.

2. The "S3" heart sound is an extra sound heard early in ventricular diastole in individuals with congestive heart failure, corresponding to the time when there is rapid filling of the ventricle with blood. One theory regarding its cause is that ventricular wall tension is increased in congestive heart failure, causing atrial blood to be forced against a relatively non-compliant ventricular wall during diastole, creating the "S3" heart sound.

3. Her history of rheumatic fever may or may not be relevant to her current symptoms. Rheumatic fever is thought to be caused by a hypersensitivity response to an infection by Streptococcus pyogenes. Certain bacterial antigens appear to be cross-reactive with antigens from human heart tissue. Hence, an immune response to the bacterium may cause unwanted destruction of human heart tissue, including the pericardium, myocardium, and endocardium. Destruction of the myocardium can, itself, lead to congestive heart failure. Destruction of the endocardium can involve the valves, though by far the most commonly affected are the valves in the left side of the heart (i.e. the mitral and / or aortic valves). Since it is Martha's pulmonic valve that is stenotic, it may be unrelated to her prior history of rheumatic fever.

4. A "normal" cardiac silhouette does not rule out a problem with Martha's heart. Her pulmonic stenosis creates more resistance to the outflow of blood from the right ventricle into the pulmonary artery. Over time, the right ventricle will undergo concentric hypertrophy in an attempt to generate stronger contractions to overcome this resistance to flow. In concentric hypertrophy, the thickness of the wall increases, but the overall diameter of the ventricle does not change much. Since Martha's ventricular diameter hasn't changed much, the silhouette appearance of her heart on a chest X-ray will not be enlarged.

5. Martha's hepatomegaly and moderate ascites are caused by increased systemic venous pressure. Since there is resistance to the flow of blood out of the right ventricle into the pulmonary artery, hydrostatic pressure rises in Martha's right ventricle, right atrium, and central systemic veins (this is why her jugular veins appear distended). This build-up of hydrostatic pressure is reflected backwards into her more peripheral systemic veins - - thus pressure rises in the inferior vena cava and hepatic vein of the liver. Elevated venous pressure in the hepatic sinusoids forces water from the bloodstream into the interstitial spaces of the liver, causing the liver to become swollen. A similar build-up of systemic venous pressure forces water from the bloodstream out into the peritoneal cavity, causing "ascites."

6. The pitting edema in Martha's ankles is also caused by an elevated systemic venous pressure. Fluid escaping from the peripheral capillaries into the interstitial spaces of her legs causes them to become edematous. This condition is aggravated when Martha spends several hours of the day standing, and is alleviated to some extent when Martha lies down with her feet above heart level.

7. Support stockings will place an external pressure on Martha's lower legs, forcing some of the excess interstitial fluid into the lymphatic and blood vessels. One must be careful, however, when advising patients to wear support stockings. The stockings should place

even pressure around the entire lower legs, and should not have restrictive bands of elastic at the top. Furthermore, if the patient has atherosclerosis and blockage of arteries supplying the legs, such support stockings may actually limit arterial blood flow into the legs, and thus should not be used.

8. increased afterload because the enlarged heart and ventricle are causing the problem systemically.

9. Right-sided congestive heart failure, which classically causes systemic edema. Compare this with left-sided congestive heart failure, which causes pulmonary edema.

10. The increased afterload placed upon Martha's right ventricle decreases her right ventricular stroke volume (i.e. decreases the volume of blood pumped out of the ventricles per contraction). To maintain an adequate cardiac output (i.e. volume of blood pumped out of the heart in one minute) to meet Martha's metabolic needs, she must either (A) increase the strength of contraction (i.e. increased contractility), and / or (B) increase the heart rate (i.e. the number of contractions per minute). In either case, Martha's sympathetic nervous system coordinates the response via the baroreceptor reflex. Furthermore, since Martha's cardiac output is likely to be below that required to meet her metabolic needs, the sympathetic nervous system stimulates systemic arteriolar vasoconstriction to the "less vital" organs (e.g. those of digestion and urination) while more blood is preferentially diverted to the "more vital" organs (e.g. the heart and brain).

a. Over the long term, Martha's right ventricle will undergo concentric hypertrophy as mentioned in #4. This will allow the right ventricle to increase its strength of contraction, but there are limits to how well this mechanism works. For example, as Martha's right ventricular wall thickens, the innermost portion of it receives relatively less blood, limiting its contractile strength.

b. Reduced cardiac output will diminish blood flow to the kidneys, triggering the renin-angiotensin-aldosterone (R-A-A) axis. During this response, the hormone renin is released from the juxtaglomerular ("granular") cells of the nephrons and enzymatically converts the liver protein angiotensinogen into angiotensin I. Angiotensin I, in turn, is converted into angiotensin II by ACE (i.e. angiotensin-converting enzyme). Angiotensin II has multiple effects, most of which serve to increase the systemic arterial pressure. Angiotensin II directly causes widespread systemic arteriolar vasoconstriction (hence, its name), which increases the total peripheral resistance to blood flow, and thus also the blood pressure. It also triggers the hypothalamic release of ADH (antidiuretic hormone), a hormone that stimulates the kidneys to conserve water and produce smaller volumes of very concentrated urine, ultimately increasing total blood volume and blood pressure. Perhaps most importantly, angiotensin II stimulates the release of the hormone aldosterone from the adrenal cortex. Aldosterone stimulates tubular reabsorption of sodium ions (in exchange for hydrogen and potassium ions) in the distal renal tubules of the kidneys. The movement of sodium ions from the renal tubules back into the bloodstream is followed by the osmotic movement of water, thus increasing the systemic blood volume and blood pressure.

c. As can be seen, the R-A-A axis increases total blood volume and thus increases the pre-load placed upon Martha's right ventricle. This increase in pre-load will increase the strength of right ventricular contraction via the Frank-Starling relationship in the heart, though there are limits to the effectiveness of this heightened R-A-A axis (see answer #12).

11. Digoxin is a digitalis derivative that slows the heart rate (i.e. it is a negative chronotropic drug) and increases the contractility (i.e. it is a positive inotropic drug) of Martha's failing right ventricle, making it a more efficient pump. By blocking the Na+/K+ ATPase pump in the cardiac contractile cell membrane, digoxin increases intracellular Na+ concentration.

This, in turn, decreases the tendency of the cell membrane Na+/Ca+2 ion exchanger to move Na+ ions into the contractile cell and Ca+2 ions out of the contractile cell. The net effect of digoxin is thus to increase the concentration of Ca+2 ions in contractile cells. Cytoplasmic Ca+2 directly and indirectly helps to initiate the sliding filament mechanism of muscle contraction in contractile cells. It directly does so by binding to troponin C and uncovering the myosin globular head binding sites on actin proteins. It indirectly does so by stimulating release of additional Ca+2 ions from the sarcoplasmic reticulum into the cytoplasm. In the end, the higher the cytoplasmic Ca+2 ion concentration, the stronger and more long-lasting the ventricular contraction.

12. The activation of the R-A-A axis (as described in #10 above) may initially be a useful response, helping to increase the pre-load and thus the stroke volume of the right ventricle via the Frank-Starling relationship of the heart. However, continued increases in pre-load will only increase the stroke volume up to a certain point, beyond which any further increase in blood volume can exacerbate the systemic edema and congestive heart failure.

a. At this point, it is useful to treat Martha's systemic edema with furosemide ("Lasix"), a loop diuretic which blocks the active transport of sodium ions from the loop of Henle back into the bloodstream. Since less sodium is reabsorbed, less water follows by osmosis. This will increase Martha's urinary output and help her to excrete some of the excess sodium and water from her interstitial fluid.

b. Martha's high blood pressure places an increased workload ("afterload") on her heart. Her physician may prescribe an "ACE inhibitor" medication (e.g. captopril, enalopril) to block the conversion of angiotensin I to angiotensin II. This will effectively slow down the R-A-A axis and significantly reduce her systemic arterial blood pressure, allowing her ventricles to function more efficiently.