Study Guide- Alterations of Cardiovascular Function
Decreasing levels of LDL can cause regression of atherosclerotic lesions and can
improve endothelial function.
The oxidation of LDL is an important step in atherogenesis. Inflammation with
oxidative stress and activation of macrophages is the primary mechanism.
Oxidized LDLs are toxic to endothelial cells, cause smooth muscle proliferation,
and activate further immune and inflammatory responses.
What alteration occurs in injured endothelial cells that contributes to
atherosclerosis? Injured endothelial cells become inflamed and cannot make
normal amounts of antithrombotic and vasodilating cytokines.
What factor is responsible for the hypertrophy of the myocardium associated with
hypertension? Angiotensin II is responsible for the hypertrophy of the
myocardium and much of the renal damage associated with hypertension.
Atherosclerosis causes an aneurysm because:
Atherosclerosis is a common cause of aneurysms because plaque formation erodes
the vessel wall.
Pulmonary emboli originate in the venous circulation (mostly from the deep veins
of the legs) or in the right heart.
Buerger disease is an inflammatory disease of the peripheral arteries.
Inflammation, thrombus formation, and vasospasm eventually can occlude and
obliterate portions of small and medium-size arteries. Typically affected are the
digital, tibial, and plantar arteries of the feet and the digital, palmar, and ulnar
arteries of the hands.
Raynaud phenomenon and Raynaud disease are characterized by attacks of
vasospasm in the small arteries and arterioles of the fingers and, less commonly,
the toes.
Coronary artery disease (CAD) can diminish the myocardial blood supply until
deprivation impairs myocardial metabolism enough to cause ischemia, a local state
in which the cells are temporarily deprived of blood supply. They remain alive but
cannot function normally. Diabetes mellitus is an extremely important risk factor for
CAD.
Hypertension is responsible for a two- to threefold increased risk of atherosclerotic
cardiovascular disease.
Low levels of HDL cholesterol also are a strong indicator of coronary risk,
whereas high levels of HDLs may be more protective for the development of
atherosclerosis than low levels of LDLs.
Cardiac cells remain viable for approximately 20 minutes under ischemic
conditions. If blood flow is restored, aerobic metabolism resumes, contractility is
restored, and cellular repair begins. If the coronary artery occlusion persists beyond
20 minutes, myocardial infarction occurs.
Most individuals with acute pericarditis describe several days of fever, myalgias,
and malaise followed by the sudden onset of severe chest pain that worsens with
respiratory movements and with lying down. Although the pain may radiate to the
back, it is generally felt in the anterior chest and may be confused initially with the
pain of acute myocardial infarction. Individuals with acute pericarditis also may
report dysphagia, restlessness, irritability, anxiety, and weakness.
Mitral valve prolapse tends to be most prevalent in young women. Studies suggest
an autosomal dominant and X-linked inheritance pattern. Because mitral valve
prolapse often is associated with other inherited connective tissue disorders (e.g.,
Marfan syndrome, Ehlers-Danlos syndrome, osteogenesis imperfecta), it is thought
to result from a genetic or environmental disruption of valvular development
during the fifth or sixth week of gestation.
Infective endocarditis is a general term used to describe infection and inflammation
of the endocardium—especially the cardiac valves. Bacteria are the most common
cause of infective endocarditis, especially streptococci, staphylococci, or
enterococci.
Right heart failure is defined as the inability of the right ventricle to provide
adequate blood flow into the pulmonary circulation at a normal central venous
pressure. It most often results from left heart failure when the increase in left
ventricular filling pressure that is reflected back into the pulmonary circulation is
severe enough. As pressure in the pulmonary circulation rises, the resistance to
right ventricular emptying increases.