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Congestive Heart Failure Case Study
Anatomy and Physiology Review
http://www.nhlbi.nih.gov/health/health-topics/topics/hhw/printall-index.html
Background Pathophysiology
What 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:
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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 extremities
o A history of hypertension, diabetes, obesity, heart valve malfunctions, and
previous heart disease all increase your chances for developing CHF.
Physical examo 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 abdomen
o 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 failure
o CBC, PT/PTT, BMP
o Bun/Cr levels
o ABG
Imaging –
o A chest x-ray – can show fluid in lungs, increased heart size or other
abnormal findings
o 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 Series
EKG
CBC with differential
BNP Blood Test or CRP Test
Thyroid Panel Test
Doppler Ultrasound
Echocardiography
Stress Test
Holter Monitor
Diagnosis:
Left Sided Heart Failure
Differential Diagnosis:
Hypothyroidism
Right Sided Heart Failure
Referral:
Cardiologist
Nutritionist/Trainer
Follow-up: 2 Weeks
Diagnostic Results
Chest X-Ray
http://www.radiologyassistant.nl/en/4c132f36513d4
BNP Blood Test
http://www.chfpatients.com/tests/bnp.htm#bnp_levels
http://www.heart-strong.com/files/heartstrong-BNParticleWebsite_1_.pdf
Patient Name: Martha Jones Age 54
Sex: Female
BNP Levels 695 pg/mL
CRP Test
http://my.clevelandclinic.org/heart/services/tests/labtests/crp.aspx
EKG
Doppler Ultrasound
Angiocardiography
Echocardiogram
http://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. angiotensinconverting 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.