Download Case Study 1 Can Mr. H.`s brother`s heart recover? There are some

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Transcript
Case Study 1
Can Mr. H.’s brother’s heart recover?
There are some things we need to understand about heart muscle. Once heart muscle is dead or
infarcted it does not regenerate to normal tissue. Therefore, we can only limit effects that this
malfunction has on the rest of the body, restore circulation to the area of infarction ASAP, and
prevent further complications. Thus we get the idea of time=muscle.
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The infracted material is surrounded by a zone of hypoxic muscle and this may progress
to necrosis, undergo remodeling or return to normal.
Myocardial remodeling causes myocardial hypertrophy and loss of contractile function of
the heart muscle distal to the area of infarction. This remodeling is limited when we
restore blood flow quickly and use ACEI and beta-blockers post MI.
After six weeks, the necrotic area is replaced by scar tissue- it is strong but can’t relax
and contract like healthy myocardial tissue (McCance & Huether, 2006).
I would tell Mr. H. that there is a lot that his brother and health care provider can be doing to
reduce his risk of poor outcomes post MI. Prognosis post MI depends on MANY factors. Here
are a few things that will determine how Mr. H.’s brother will recover.
Type of MI…
For example, the landmark Framingham Heart study of the late 80’s and 90’s compared Q wave
MI’s to non Q-wave MI’s.
The Non-Q-wave group (non-transmural- less initial damage):
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Had a 1.8 times more risk of re-infarcting
Baseline hypertension increases risk of re-infarction
Higher rates of unstable angina
The Q wave group (transmural):
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Higher rates of congestive heart failure (Berger, Murabito, Evans, Anderson & Levy,
1992)
Drugs that you are on post-MI…
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Beta blockers can improve survival by 20-25% through preventing cardiac mortality and
reinfarction
Antiplatelet agents like aspirin can reduce risk of reinfarction and/or stroke by 25%
Lipid lowering therapy
Angiotensin converting enzyme inhibitors (ACEI) can decrease risk of reinfaraction and
mortality (Kaski & Fernandex-Berg, 2008).
Lifestyle…
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Smoking
Diet
Exercise (Skinner, Cooper & Feder, 2007)
Cardiac rehabilitation…
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When offered with an exercise component this reduces cardiac mortality (Skinner,
Cooper & Feder, 2007).
Other comorbidites…

Patients with advanced age, low left ventricular ejection fraction, arrhythmia, increased
heart rate, elevated BUN, hypertension and diabetes (can double mortality) tend to do
worse post MI. These conditions narrow in on two big metabolic disorder consequenceshigh lipids and activation of the SNS and renin-angiotensin systems (Abraham, 2003).
Depression post MI….
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With the prevalence of major depression approx. 1 in 5 in MI patients who are
hospitalized, this is a significant issue
Depression appears to be associated with about a three-fold increased risk of cardiac
mortality
Depression post MI is inversely related physical quality of life, to social life quality of
women, return to work for employed men, and sexual activity and satisfaction (AHRQ,
2005).
So up for discussion and further research:
Can you think of other factors affecting prognosis post acute MI that are of interest to the
nurse practitioner?
At what point should a client be managed by a cardiologist vs. a primary health care
provider? Or is a multidisciplinary approach better?
References
Abraham, W.T. (2003). Diabetes, hypertension, and renal insufficiency in post-myocardial
infarction cardiovascular risk. Reviews in Cardiovascular Medicine, 4(supp3): S30-S36.
AHRQ (2005). Post-myocardial infarction depression. Evidence Based Practice. Retrieved
February 22, 2009 from http://www.ahrq.gov/clinic/epcsums/midepsum.pdf
Berger, C.J., Murabito, J.M., Evans, J.C., Anderson, K.M., & Levy, D. (1992). Prognosis after
first myocardial infarction [online version]. Journal of the American Medical Association
268(12).
Kaski, J.C., & Ferdnandez-Berger, D. (2008). Secondary prevention after acute myocardial
infarction and coronary revascularization: Focus on angiotensin converting enzyme inhibitors.
Cardiovascular Drug Therapy, 22: 185-191.
McCance, K., & Huether, S., (2006). Pathophysiology: The biologic basis for disease in adults
and children. St. Louis Missouri: Mosby.
Skinner, J.S., Cooper, A., & Feder, G.S. (2007). Secondary prevention for patients following a
myocardial infarction: summary of NICE guidelines. Heart, 93: 862-864.