Month: January 2014

Improving Survival After Myocardial Infarction

A 78-year-old man comes to the physician because of a 6-month history of mild to moderate shortness of breath when climbing stairs. He had a myocardial infarction 2 years ago and has had an ejection fraction of 30% since then. His only medication is a β-adrenergic blocking agent. The lungs are clear to auscultation. Cardiac examination shows an S4 gallop. There is no peripheral edema. Laboratory studies are within normal limits. An ECG shows no acute changes. Which of the following is the most appropriate pharmacotherapy?

A) α-Adrenergic blocking agent

B) Angiotensin-converting enzyme (ACE) inhibitor

C) Angiotensin2-receptor blocking agent

D) Nitrates

E) Thiazide diuretic

F) Aspirin

G) α-Adrenergic Agonist

H) Furosemide

I) Digoxin

J) Warfarin

K) Enoxaparin

Through multiple studies we have come to understand that Beta blockers have been shown to improve survival after myocardial infarction (MI) by decreasing both oxygen demand and the incidence of ventricular arrhythmia. The patient in the vignette above is already on a Beta blocker, what other medication would be most appropriate?

Angiotensin-converting enzyme (ACE) inhibitors such as enalapril, have been shown to improve survival in post-MI patients who have ejection fractions less than 40%. A low ejection fraction will cause a myriad of consequences, one in particular (pre-renal azotemia  acute kidney injury (AKI).

It is our duty as medical doctors to take additional measures to limit infarct size and to reduce remodeling we do this with the use of nitroglycerin or angiotensin-converting enzyme (ACE) inhibitors.

Nitroglycerin can limit infarct size, infarct expansion and remodeling, but large-scale studies have not demonstrated clear mortality benefit following acute MI (1). However, clinical trials have shown that ACE inhibitors can improve survival in patients with reduced LV systolic function or heart failure after MI as well as reduce remodeling and left ventricular dilation (LVD) (2). Initial evidence that ACE inhibitors attenuated LV dilatation after MI came from studies in selected patients with LV impairment, anterior MI or Q-wave MI (3). However, evidence that ACE inhibitor treatment improves LV remodeling in patients with a patent IRA and in studies in which high proportions of patients received thrombolysis has been conflicting (4). Benefit from ACE inhibitor treatment thus seems to be greatest in patients at higher risk of LV dilatation due to more extensive infarction, particularly those with anterior or Q-wave infarction with an occluded IRA.

1. ISIS-4 Collaborative Group.  ISIS-4. a randomised factorial trial assessing early oral captopril, oral mononitrate, and intravenous magnesium sulphate in 58,050 patients with suspected acute myocardial infarction. Lancet. 345 1995:669-685.

2. Pfeffer  M., Braunwald  E., Moye  L.; Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infarction. results of the Survival and Ventricular Enlargement Trial. N Engl J Med. 327 1992:669-677.

3. Sharpe  N., Murphy  J., Smith  H., Hannan  S.; Treatment of patients with symptomless left ventricular dysfunction after myocardial infarction. Lancet. 1 1988:255-259.

4. French  J.K., Amos  D.J., Williams  B.F.; Effects of early captopril administration after thrombolysis on regional wall motion in relation to infarct artery blood flow. J Am Coll Cardiol. 33 1999:139-145.

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QUIZ: Patient Management

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You are working late night when a previously healthy 4-year-old girl is brought in  to the ED because of fever and refusal to walk for 1 day. She appears mildly ill. Her temperature is 38.6 C (101.5 F), pulse is 120/min, and respirations are 22/min. The right knee is erythematous and swollen. She holds her right knee in flexion and resists any attempted movement of her right leg. She cries when the right knee is moved. Which of the following is the most appropriate next step in management?

A) Acetaminophen with codeine therapy

B) Arthrocentesis

C) Bone marrow aspiration

D) Bone scan

E) Immobilization and traction

F) Lyme titer

G) MRI of the spine

H) Physical therapy

I) Reassurance

J) Serum rheumatoid factor assay

K) Systemic antibiotic therapy

Infections of the joints (known as septic arthritis, pyogenic arthritis, suppurative arthritis, purulent arthritis, or pyarthrosis) have many causes i.e, bacteria, fungi, mycobacteria, and viruses. However, the term “septic arthritis” usually refers to bacterial arthritis or fungal arthritis, but bacterial joint infections are most common.

Bacterial arthritis is a medical emergency and requires prompt recognition and management. Any delays in treatment are often associated with long-term sequelae. These sequelae can have major lifelong impact if a major weight-bearing joint is involved, particularly when the hip joint is involved in infants.

As such, the goals of treatment include sterilization and decompression of the joint space and removal of inflammatory debris to relieve pain and prevent deformity or functional sequelae. Surgical drainage and antimicrobial therapy are the cornerstones of therapy. After appropriate cultures have been obtained, empiric antimicrobial therapy should be initiated for infants and children with characteristic clinical and laboratory features of bacterial arthritis.

A Short Read On: Adrenocorticotropic Hormone

A Short Read On The Neuroendocrine Response Of Adrenocorticotropic Hormone In Shock
By C.M Diaz
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Introduction: Severe pain or acute stress causes the hypothalamic activation and release of adrenocorticotropic hormone (ACTH). Our natural response is to counteract this stress with some sort of physiologic compensation in order to return or maintain homeostasis.

Today I want to discuss briefly the neuroendocrine response of ACTH to the clinical syndrome of shock (which is defined by Harrison’s 18th Edition; as the clinical syndrome that results from inadequate tissue perfusion – irrespective of the cause).

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