NURSING 3PA2 Study Guide - Final Guide: Inotrope, Stenosis, Gruel

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2 May 2016
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N2PF3 Module 7: Alterations in Cardiovascular Function
MODULE 7: ALTERATIONS IN CARDIOVASCULAR FUNCTION
Learning Objectives
Recall the pathophysiology of atherosclerosis
Define ischemia
List the common causes of ischemia
Describe the pathophysiology of ischemia
Differentiate between ischemia, injury, and infarction
Define heart failure
Discuss the pathophysiology of right and left heart failure
Relate the clinical manifestations of heart failure to the pathophysiology
Discuss the current management strategies for heart failure
Atherosclerosis Review
Atherosclerosis: hardening of the arteries
Atheros”: “gruel” or “paste” and “Sclerosis”: “hardness”. Thus, the term denotes the formation of fibrofatty
lesions in the intimal lining of the large and medium-sized arteries.
Characterized by: the development of atheromatous lesions within the intimal lining of the arteries that
protrude into and eventually obstruct blood flow
Development of atherosclerosis
1. Endothelial cell injury:
-Normal endothelium is smooth, with very tight junctions between cells. Endothelium injury occurs due
to smoking, elevated LDL (hyperlipidemia), immune mechanisms, and mechanical stress associated with
hypertension. Hemodynamic factors may also play an important role, as evidenced by the fact that
atherosclerotic lesions tend to form where vessels branch, or in areas of turbulent flow. Other factors
that can cause injury are hyperhomocystenemia, toxins and viruses
-Injury causes the release of inflammatory cytokines which attract leukocytes (i.e. monocytes) and
platelets to the site of inflammation
-Endothelial cell injury turns on the expression of adhesion molecules and monocytes become sticky and
attach themselves to the endothelium.
-In response to leukocyte binding, the endothelium produces less anti-thrombotic and vasodilating
cytokines which contributes to narrowing of arteries
2. Monocyte emigration
-Monocytes adhere to the endothelium and migrate between the cells to localize in the intima,
-Once they pass through the endothelial layer and into the subendothelial space, monocytes are activated
and transformed into macrophages, and free radicals (i.e. toxic oxygen species) are released
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N2PF3 Module 7: Alterations in Cardiovascular Function
3. LDL oxidation
-LDL makes its way through the endothelium and is oxidized into proinflammatory lipid by free radicals
-Oxidized LDL serves as an attractant to monocytes in the endothelium, causing further migration of
monocytes into the subendothelium
oSpecifically, oxidized LDL provides a signal that is recognized by surface receptors on the
macrophages, and an inflammatory response is triggered, causing release of prostaglandins,
leukotrienes and cytokines. This attracts more monocytes to move into the sub-endothelial
spaces and promotes their differentiation into activated macrophages.
-Oxidized LDL is toxic to the endothelium and causes endothelial loss and exposure of the sub-
endothelial tissue to blood components. Likewise, the inflammatory response which has now been
initiated causes further endothelial cell injury. This leads to platelet adhesion and aggregation and fibrin
deposition
-Oxidized LDL is consumed by activated macrophage which turns them into foam cells. Foam cells then
release growth factors and inflammatory cytokines that worsen endothelial injury and further the
process of atherogenesis.
4. Smooth muscle proliferation
-Injury causes exposure of the subendothelium which causes aggregation and adherence of platelets.
-Macrophages, foam cells and platelets produce growth factors that contribute to the migration and
proliferation of smooth muscle cells and the elaboration of the extracellular matrix. This causes the
endothelial layer to pouch out which further contributes to narrowing of the arteries
5. Formation of fatty streak
-Lipids continue to accumulate beneath the endothelial layer
-Macrophages and smooth muscle cells that have become distended with lipid to form foam cells
accumulate to form fatty streaks (thin, yellowish discolorations), which progressively enlarge and
occlude the vessel lumen.
6. Formation of fibrofatty atheroma with a lipid core
-Lipids accumulate beneath the endothelial layer and form a hard, lipid core. As enzymes eat away at the
protective fibrous cap, the atherosclerotic plaque becomes vulnerable to rupture
7. Plaque hemorrhage
-Both smooth muscle and foam cells in the lipid core contribute to the expression of tissue factor in
unstable plaques.
-When a plaque ruptures, there is exposure of substances from the lipid core which provide a stimulus
for platelet aggregation and thrombus formation
-Once exposed to blood, tissue factor initiates the extrinsic coagulation pathway, resulting in the local
generation of thrombin and deposition of fibrin.
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N2PF3 Module 7: Alterations in Cardiovascular Function
-Once a thrombus forms, blood flow through the coronary artery, to the myocardium can be
compromised, and in some cases, completely obstructed, leading to infarction.
Myocardial Ischemia
Myocardial ischemia
Occurs when the ability of the coronary arteries to supply blood is inadequate to meet the metabolic
demands of the heart, i.e. imbalance between myocardial oxygen supply and demand.
Angina is reversible if blood flow is restored before cellular damage occurs.
Myocardial oxygen supply and demand:
Myocardial oxygen supply is regulated by:
-The patency (i.e. size of the lumen) of the coronary vessel
-The ability of ventricular wall to compress; and
-Amount of time the ventricle spends in diastole. Diastole is the portion of the cardiac cycle when the
ventricle is in a relaxed state, stretching as it fills with blood from the atrium. Blood flow to the
subendocardial muscle is greatest during diastole.
Myocardial oxygen demand is dependent upon:
-Myocardial contractility
oMyocardial contractility is the intrinsic ability of the heart muscle to shorten (i.e. contract) and
generate force.
oAs myocardial contractility increases, the rate of change in wall stress increases, which in turn
increases myocardial oxygen uptake (i.e. increased demand)
-Heart rate:
oAs the heart rate increases, myocardial oxygen demand and consumption also increases.
oAs the heart rate increases, there is decreased diastolic filling time and thus reduced
subedocardial coronary blood flow
-Amount of ventricular wall stress.
oIncreased wall stress increases myocardial oxygen demand
oVentricular wall stress may be the product of preload or afterload.
Preload is the distending force of the ventricle wall (i.e. the volume in the ventricle just
before it contracts), which is highest at the end of diastole, just before contraction.
Afterload is the load against which the heart must contract to eject blood – i.e. the
amount of resistance the ventricle must overcome in order to contract.
oClinical considerations: Because wall stress is inversely related to wall thickness, ventricular
hypertrophy serves as an adaptive mechanism by which the ventricle is able to offset the
increase in wall stress.
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