Stepped Care Plans –

         Over the past two decades, the concept of progressive stepped care has evolved from a narrow set of incremental options to a broader set of guidelines for nursing practitioners’ and treating physicians, by the Joint National Committee on Hypertension Vl ³²  (JNCH Vl):   

• Step 1 – Prescribe lifestyle modifications, including weight reduction, moderated alcohol intake, regular physical exercise, reduced sodium intake, and smoking cessation.
• Step 2 – If response is inadequate, continue the lifestyle modification,  and add mono-therapy for mild to moderate (stage 1-2) hypertension with thiazide diuretics or β -blockers, unless there is a contraindication.  Other agents {e.g., angiotensin-converting enzyme (ACE) inhibitors, calcium antagonists, α-blockers, and α-β-blockers} are satisfactory substitutes for patients with contraindications, although the long-term net benefits of these medications are not fully established. 
• Step 3 – If response to initial treatment is inadequate, increases medication dose, substitute another anti-hypertensive drug, or add a second agent from a different drug class. 
• Step 4 – If response is still inadequate, add a second or third agent from a different drug class.  Including an appropriate diuretic (if not already administered). 

         Note: In the spirit of academic fullness, the author has read through the entire manuscript  and found a lack or limited sensitivity to three important issues:  First, was the hemodynamic diversity among hypertensives, also secondly, the negative metabolic effects of thiazides and β-blockers, and thirdly, the need for direct testing of stepped care versus alternative approaches.  The author’s final thought on the original published manual from JNCH Vl:  Use this manuscript as a guideline only, and tailor the “Steps” to your own needs, due to the variables of patients and environmental surroundings. 

Conclusion;  

 Looking Toward the Near Future –       

     As one tries to think about the future of hypertension profiling and management, there will continue to be exciting developments in three major areas.  The author believes:  first, basic science advances in molecular and genetic medicine will likely shed light on the initial and initiating events that cause the deranged physiology of hypertension.  Secondly, evolving insights from epidemiology will refine definitions of high-risk groups and clustering to focus efforts that produce the greatest positive yield for a population, despite resource constraints.  Finally, the development of more effective and better-tolerated anti-hypertensive medications will almost certainly combine with more sophisticated behavioral approaches to enhance adherence.   Patients may indeed, enjoy a fuller and more beneficial life style with less risk reductions while under the care and medication management protocol. 

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[2]Baum, D., Kennedy, DL. Knapp, EE. et al.  Prescription drug use in 2001, and changes over time.  Med Care 2002; 27: 105-113. Cited again in 2008, revised edition, ACP Medicine Textbook of Cardiovascular Medicine:  © 2008, by Lippincott Williams & Wilkins Publishing Co.  

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[5] Segall, HN.  How Korotkoff, the surgeon, discovered the auscultatory method of measuring arterial pressure.  Ann Intern Med 1975; 83: 561-562.

[6] Goldblatt, H., Lynch, J., Hansel, RF.  et al.  Studies on experimental hypertension. I.  The production of persistent elevation of systolic blood pressure by means of renal ischemia.  J Exp Med 1943; 59: 347-379.

[7] Page, IH. The mosaic theory of hypertension.  In Bock KD, Cottier, PT, Eds.  Essential hypertension.  Berlin:  Springer-Verlag, 1960: 1-9.  Also, cited in:  Hypertension, Amer H Assoc 1991; 18; 443-445.  http://hyper.ahajournals.org//

[8] Hamet, P., Pausova, Z., Adarichev, V., et al.  Hypertension:  genes and environment.  J Hypertens 1989; 16: 397-418.

[9] Brown, M.J. The causes of essential hypertension.  Br J Clin Pharmacology 2000; 42:21-27.

[10] Williams, R., Hunt, S., Hopkins, P., et al.  Genetic basis of familial dyslipidemia and hypertension:  15-year results from Utah.  Am J Hypertens 2000; 7: 319S-327S.

[11] Williams, R., Hunt, S., Hopkins, P., et al.  Genetic basis of familial dyslipidemia and hypertension: 

[12] Elliott, P., Stamler, J., Nichols, R., et al.  INTERSALT revisited further analyses of 24-hour sodium excretion and blood pressure within and across populations.  B M J 2001; 312:  1248.

[13] Sacks, F., Svetkey, L., Vollmer, W., et al.  Effects on blood pressure of reduced dietary sodium and the dietary approaches to stop hypertension (DASH) diet.  N Engl J Med 344:3, 2006. 

[14] Krauss, R., Eckel, R., Howard, B., et al: AHA dietary guidelines:  revisions 2000; a statement for healthcare professionals from the nutritional committee of the American Heart Association.  Circul 102: 2284, 2000.  Cited again, in 2007; AHA, dietary guidelines, revisited @ http://americanheart,org/dietary guidelines// 

 

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