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Case Study 1- Unit 8
Group 1 Post by Andria Marin, Joanna James, and Lorna Estabrooks
You discuss with Mr. H the damage to his heart. You want to impress upon him the other end
organ damage that occurs with untreated hypertension.
What Clinical Signs and symptoms might there be?
Now that Mr. H is aware of the potential harms of end organ damage that may occur with
untreated hypertension it is important for him to know the clinical signs and symptoms he needs
to watch for in order to know when to seek appropriate medical help.
CNS: Brain- Sustained hypertension can cause damage to endothelium thereby reducing blood
vessel diameter, potentiating further atherosclerosis, and promoting platelet aggregation. As a
result a reduction in blood flow and oxygen may occur, leading to TIA’s, acute brain infarct,
cerebral thrombosis, and aneurysms (McCance and Huether, 2006). The latter may be exhibited
by changes in vision or speech, dizziness, weakness, sudden falls, and temporary paralysis on
one side (Smeltzer &Bare, 2000).
Eyes (retinas)-Reduced blood flow and high arteriolar pressures can result in
hemorrhages, vision changes, fluid accumulation, exudates, small infarctions, and in severe
hypertension papilledema (McCance & Huether; Smeltzer & Bare, 2000).
CVS: Myocardium- an increase in workload leads to left ventricular hypertrophy. Untreated, the
strain on the heart working against high pressure system contributes to heart failure overtime.
Heart failure may lead to congestive heart failure manifested by poor CO, poor systemic
perfusion, dyspnea on exertion, dizziness, confusion, fatigue, and reduced urine output (Smeltzer
& Bare, 2000).
Coronary Arteries- Damage to endothelium due to hypertension releases cytokines
mediated by the inflammatory response as a result vascular remodeling leading to narrowing of
coronary arteries occurs, as with atherosclerosis (McCance & Huether, 2006). CAD can lead to
ischemia and infarction manifested by angina, shortness of breath, nausea, vomiting, diaphoresis,
decreased blood pressure (with infarction), anxiety, increased pulse, and jugular venous
distention (Thompson, McFarland, Hirsch, & Tucker, 2002).
Aorta- hypertension weakens the vessel wall creating an outpouching potentially leading
to a dissecting aneurysm (McCance & Huether, 2006). A dissected aneurysm is manifested by a
sharp pain located in the area of the dissection; anterior chest pain is associated with ascending
aorta while back pain is associated with descending aorta (Thompson et al., 2002).
Arterial vessels of lower extremities- contribute to cool extremities, and fatigue to legs
resulting from poor perfusion due to reduced blood flow, and potential for gangrene (McCance
& Huether, 2006).
GU: Kidneys-Dysfunctions in the rennin-angiotensin-aldosterone system leading to increased
peripheral resistance that may reduce their oxygen supply and create a high pressure system in
the renal arterioles (McCance and Huether, 2006). Damage to the kidneys may lead to
nephrosclerosis followed by renal failure. This may be manifested by proteinuria and hematuria
found on urinalysis, an increase in Cr, BUN, and K+, nocturia, and decreased urine output as
renal failure progresses (Thompson et al., 2002).
McCance, K.L., & Huether, S.E. (2006). Pathophysiology the biologic basis for disease in adults
and children. (5th edition). Salt lake City, Utah: Elsevier Mosby.
Smeltzer, S.G., & Bare, B.G. (2000). Textbook of medica-surgical nursing. (9th
edition).Philadelphia: Lipincott.
Thompson, J.M., McFarland, G.K., Hirsch, J.E., & Tucker, S.M. (2002). Mosby’s clinical
nursing (5th edition). St Louis: Mosby.