Ch. 18 Final Exam (HSC 4555)

atherosclerosis

It results from accumulation of fatty deposits in the walls of coronary arteries, leading to formation of fibrous tissue in the vessel wall. (Ch. 18- Alterations in Cardiac Function)

lipoproteins

Lipids are transported through the bloodstream in combo with specific proteins (apoproteins); certain lipid-protein molecules (_________________) are associated w/ a greater risk of *atherosclerosis.* (Ch. 18- Alterations in Cardiac Function)

inflammatory, leukocytes, proliferation

Macrophages and foam cells release ____________________ mediators and growth factors that attract more ________________ and stimulate smooth muscle ____________________. (Atherosclerotic plaque formation) (Ch. 18- Alterations in Cardiac Function)

mitral stenosis

characterized by a large left atrial-to-left ventricular pressure gradient during ventricular diastole; leads to left atrial and pulmonary congestion (Ch. 18- Alterations in Cardiac Function)

mitral regurgitation

characterized by large V waves in the left atrial pressure tracing and a loud systolic murmur that radiates to the left axilla; increases the work of the left atrium and ventricle and can lead to left-sided heart failure (Ch. 18- Alterations in Cardiac Function)

mitral regurgitation (insufficiency)

characterized by the backflow of blood from the left ventricle to the left atrium during ventricular systole (Ch. 18- Alterations in Cardiac Function)

regurgitation (insufficiency)

inability of a valve to close completely, thereby allowing blood to flow backward across the valve when no flow should be occurring (Ch. 18- Alterations in Cardiac Function)

plaque, alternative, stable angina pectoris

one of the factors that impacts rate of coronary perfusion, which can lead to ischemia *Advanced* fibrous __________ is thought to produce intermittent ischemia when 75% or more of the lumen is occluded. Because they progress slowly over the years, the heart can develop ________________ pathways for myocardial blood flow. Therefore, stable fibrous plaque may produce no symptoms of ischemia unless demand of heart for O2 is suddenly elevated (exercise/stress) This leads to what type of angina? (Ch. 18- Alterations in Cardiac Function)

clot, vulnerable

one of the factors that impacts rate of coronary perfusion, which can lead to ischemia Acute coronary syndrome (ACS) occurs when *sudden* obstruction of coronary blood flow results in acute MI-- usually associated w/ formation of a ________ in coronary artery at a site of a ________________ plaque. (Ch. 18- Alterations in Cardiac Function)

auregulation

one of the factors that impacts rate of coronary perfusion, which can lead to ischemia; Failure of endothelial cells to appropriately regulate flow (_________________) is a potential mechanism for myocardial ischemia. These endothelial cells can be damaged by circulating toxins from cigarette smoke, immune cells, and infectious agents. (Ch. 18- Alterations in Cardiac Function)

aortic

one of the factors that impacts rate of coronary perfusion, which can lead to ischemia; Fall in _________ blood pressure can significantly reduce coronary perfusion, particularly in vessels w/ high resistance to flow. Can be due to shock, hemorrhage, anesthesia, which results in low BP *(poor perfusion pressure)* (Ch. 18- Alterations in Cardiac Function)

vasospasm, variant or prinzmetal angina

one of the factors that impacts rate of coronary perfusion, which can lead to ischemia; usually occurs in areas of atherosclerotic plaque, but also mechanism of ischemia in patients who have angina signs/symptoms but no significant amount of fibrous plaque in coronary arteries; can occur in response to certain drugs s/a cocaine Angina related to this is called what? (Ch. 18- Alterations in Cardiac Function)

stable angina (classic or typical), rest

type of angina pectoris; characterized by stenotic atherosclerotic coronary vessels that reduce coronary blood flow to a critical level; Onset of angina pain *predictable* and elicited by similar stimuli each time This is generally relieved by _________ and nitroglycerin (causes coronary and peripheral vasodilation --> reduces preload--> reduces myocardial workload). (Ch. 18- Alterations in Cardiac Function)

prinzmetal variant angina

type of angina pectoris; characterized by unpredictable attacks of angina pain; onset of ischemic symptoms unrelated to physical or emotional exertion, heart rate, etc *vasospasm probably mechanism* (Ch. 18- Alterations in Cardiac Function)

acute coronary syndrome (ACS)

unstable angina and myocardial infarction are both lumped together as this-- both characterized by chest pain that may be more severe and lasts longer than typical angina; umbrella term for situations where the blood supplied to the heart muscle is suddenly blocked. (Ch. 18- Alterations in Cardiac Function)

myoglobin, troponin, creatine kinase

Elevated serum levels (serum markers) of _______________, ______________, and ____________________ are indicators of MI. (Ch. 18- Alterations in Cardiac Function)

inflammation and scaring, calcification, congenital malformations

Endocardial and valvular structures may be damaged by what 4 processes? (Ch. 18- Alterations in Cardiac Function)

plaque, thrombosis, unstable angina, MI

*Acute coronary syndrome (ACS)* has an abrupt onset and is associated w/ acute changes in ____________ morphology and _________________--includes ___________________ and ________ (combined together). (Ch. 18- Alterations in Cardiac Function)

volume, blood

*Regurgitation* (insufficiency) results in extra ___________ work for the heart because more __________ must be pumped to maintain adequate flow foward. (Ch. 18- Alterations in Cardiac Function)

rheumatic heart disease, calcification

*Stenosis* is primarily due to postinflammatory scarring from _______________________________ and valvular __________________ w/ aging as primary cause. (Ch. 18- Alterations in Cardiac Function)

unstable angina

*Vulnerable plaques* in atherosclerosis are associated w/ acute coronary syndrome (ACS), or _____________________, or MI, as well as sudden cardiac arrest, and is nearly always associated w/ an acute disruption of a vulnerable plaque. (Ch. 18- Alterations in Cardiac Function)

plaques, rupture

A major aim of therapy for coronary heart disease is to stabilize ____________, making them less prone to _____________. (Ch. 18- Alterations in Cardiac Function)

atherosclerosis

About 75% of coronary-related mortalities are the result of ______________________. (Ch. 18- Alterations in Cardiac Function)

lipid core

After macrophages and foam cells release inflammatory mediators and growth factors that attract more leukocytes, excess lipid and debris begins to accumulate within the vessel wall and coalesce into a pool called a ________________. (Atherosclerotic plaque formation) (Ch. 18- Alterations in Cardiac Function)

STEMI, full, NSTEMI, less than full

An elevated ST segment in an ECG-- called ___________ is a _________ thickness injury. Absence of an ST elevation is called ____________ and is a _________________ thickness injury. (Ch. 18- Alterations in Cardiac Function)

coronary heart disease

It is the most common type of heart disease, and the leading cause of death in the USA. (Ch. 18- Alterations in Cardiac Function)

sudden cardiac death

Any of the coronary heart symptoms (angina pectoris, ischemic cardiomyopathy, unstable angina, MI) may precipitate __________________________ and associated dysrhythmias (Ch. 18- Alterations in Cardiac Function) .

Thrombus, vasospasm, Endothelial

Atherosclerosis causes narrowing of the arterial lumen that can lead to cardiac ischemia through: - ______________ formation - Coronary __________________ - ________________ cell dysfunction (Ch. 18- Alterations in Cardiac Function)

injury, endothelium, stress (hypertension), cigarettes, cytokines, hyperlipidemia

Atherosclerotic plaque formation is *initiated* by __________ to coronary artery ___________________; this can be due to: - Chronic hemodynamic wall __________ (__________________) - Toxins from __________________ - Circulating inflammatory _______________ - _____________________ (Ch. 18- Alterations in Cardiac Function)

lipid, metabolism

Atherosclerotic plaque is composed primarily of _________-- abnormal _________________ of this could cause the development of coronary heart disease (CHD). (Ch. 18- Alterations in Cardiac Function)

lipid cores

Atherosclerotic plaques w/ large ________________ are fragile and prone to rupture. (Ch. 18- Alterations in Cardiac Function)

dysrhythmias

Atrial ________________ s/a atrial fibrillation are common in those w/ *mitral stenosis* b/c of excessive atrial volume. (Ch. 18- Alterations in Cardiac Function)

narrowing, rupture, thrombus,

Critical ________________ of coronary lumen over time or sudden _____________ of plaque followed by ______________ formation causes symptoms of *coronary heart disease* (angina, infarction, ischemic cardiomyopathy, sudden cardiac arrest) (Ch. 18- Alterations in Cardiac Function)

systole

During what phase of the heart does *mitral regurgitation* occur? (Ch. 18- Alterations in Cardiac Function)

genetic, LDL receptors, liver, liver

Extreme cases of *hyperlipidemia* occurs in those who have ____________ derangements in lipid metabolism. The most common form of this is associated w/ a defect in _____________________ on ___________ cells. Therefore, the __________ (same term) is unable to efficeintly remove cholesterol from the bloodstream --> hyperlipidemia. (Ch. 18- Alterations in Cardiac Function)

inflammation, lipid core, cap, denudation, cap, shear stress

Factors that mark increased plaque vulnerability in atherosclerosis include: 1) Active ___________________ within the plaque 2) Large ________________ with a thin _______ 3) Endothelial _________________ (erosion) w/ superficial platelet adherence 4) Fissured or ruptured _________ 5) Severe stenosis predisposing to high __________________ (Ch. 18- Alterations in Cardiac Function)

LDLs, peripheral tissues, endocytosis

High levels of __________, which are high in cholesterol, are associated w/ the highest risk of atherosclerosis. They transport cholesterol to _________________________ and cholesterol uptake by these cells are mediated by receptors on these cell surfaces that bind and promote _________________ of cholesterol. (Ch. 18- Alterations in Cardiac Function)

systole, high, blowing

In *mitral regurgitation* (insufficiency), the mumur occurs throughout ventricular ____________, radiates toward the left axilla, and has a __________ (low/high)-pitched, ______________ character (Ch. 18- Alterations in Cardiac Function)

atrium, ventricle, dilate, hypertrophy, left, heart failure

In *mitral regurgitation*, both the left __________ and ________________ generally ___________ and __________________ to compensate for extra volume they are required to pump. This may eventually lead to _________-sided ___________________ (Ch. 18- Alterations in Cardiac Function)

V

In *mitral regurgitation*, elevation of left atrial volume and pressure by regurgitant flow leads to giant ______ waves on atrial pressure monitors. (Ch. 18- Alterations in Cardiac Function)

volume, SV

In *mitral regurgitation*, the left ventricle must pump a greater ___________ to compensate for regurgitant flow and maintain an effective ________. (Ch. 18- Alterations in Cardiac Function)

diastole, low, snap

In *mitral stenosis*, blood going through narrowed valve during ventricular ____________ (systole/diastole) is heard as a _________-pitched, rumbling diastolic murmur at the heart's apex; an opening _________ may be heard. (Ch. 18- Alterations in Cardiac Function)

enlargement, hypertrophy

In *mitral stenosis*, increased pressure work of the left atrium leads to atrial chamber _____________________ and _________________. (Ch. 18- Alterations in Cardiac Function)

atrial, ventricular, diastole

In *mitral stenosis*, the __________ (atrial/ventricular) remains higher than __________ (atrial/ventricular) pressure throughout _____________. (Ch. 18- Alterations in Cardiac Function)

dilate, ischemia

In *stable angina*, artherosclerotic arteries __________ poorly in response to increased myocardial oxygen requirements, so under conditions of increased myocardial workload, the perfusion is inadequate and ______________ results. (Ch. 18- Alterations in Cardiac Function)

rupture, thrombus, unstable angina, myocardial infarction

In both cases of ACS (unstable angina and MI), plaques ____________ w/ subsequent acute _______________ development. However, in ____________________, occlusion is partial or clot is dissolved before death of myocardial tissue while in _______________________, occlusion is complete and thrombus persists long enough for development of irreversible damage to myocardial cells --> necrosis. (Ch. 18- Alterations in Cardiac Function)

lower, higher

In general, the greater the percentage of *lipid* in the lipoprotein, the ____________ (lower/higher) its density. The greater the percentage of *protein* in lipoprotein, the ___________ (lower/higher) its density. (Ch. 18- Alterations in Cardiac Function)

atherosclerotic plaque, platelet, vasospasm, autoregulation, perfusion pressure

In regards to ischemia and O2 supply, *rate of coronary perfusion* can be impaired by: 1) Large, stable ___________________________________ 2) Acute ____________ aggregation 3) ________________ 4) Failure of ____________________ by microcirculation 5) Poor _________________________ (Ch. 18- Alterations in Cardiac Function)

myocardial infarction, unstable angina

In the case of ACS, if cardiac biomarkers are elevated (indicative of necrosis), diagnosis of ________________________ is made; if not, diagnosis of _______________________ is made instead. (Ch. 18- Alterations in Cardiac Function)

Q waves, inverted

Infarcted muscle that is necrotic and no longer electrically active is indicated on ECGs by abnormally deep or wide ______________ and ____________ T waves. (Ch. 18- Alterations in Cardiac Function)

chylomicrons

Inside the mitochondria and golgi apparatus of mucousal cells, fats are assembled into *water-soluble* molecules, called __________________ to be transported in the lymphatics to enter the circulatory system to the liver. (Ch. 18- Alterations in Cardiac Function)

ATP, O2, contraction

Myocardial cells are *unable* to store much __________ and therefore must continuously receive a supply of ________ for aerobic synthesis of it, or else it could lead to ischemia. It is essential for powering myocardial _______________ as well as for cell maitenance . (Ch. 18- Alterations in Cardiac Function)

cap, stable

Older plaques have significant *collagen* and *fibrin*, which form a _______ and make the plaque more ___________. (Atherosclerotic plaque formation) (Ch. 18- Alterations in Cardiac Function)

endothelial, smooth muscle, macrophages, foam cells

Once LDLs are oxidized by endothelial cells and macrophages in the coronary endothelium, they are damaging to ________________ and _____________________ cells and stimulate the recruitment of ___________________ into the vessel wall, where they engulf lipids and become ________________ (lipid-filled macrophages) (Atherosclerotic plaque formation) (Ch. 18- Alterations in Cardiac Function)

permeable, leukocytes, LDLs, insudation, oxidized

Once injury occurs to coronary artery endothelium, the endothelium becomes more _________________ and recruits _________________. _________ leak through the endothelium and into the vessel wall (called __________________) and are then ______________ by endothelial cells and macrophages. (Atherosclerotic plaque formation) (Ch. 18- Alterations in Cardiac Function)

liver

The __________ normally binds and internalizes about 75% of circulating LDL cholesterol. (Ch. 18- Alterations in Cardiac Function)

lipid, antiplatelet

Patients w/ high risk or known presence of vulnerable plaques benefit from therapies such as __________-lowering agents (to stabilize plaques) and ________________ agents (to prevent thrombosis). (Ch. 18- Alterations in Cardiac Function)

cardiac dysrhythmias, heart failure, cardiogenic shock, ventricular rupture, pericarditis, thromboembolism

Potential complications of MI are.... (6) (Ch. 18- Alterations in Cardiac Function)

left atrial, pulmonary, hypertension, right ventricular, right-sided

Progressive narrowing of the mitral valve in *mitral stenosis* leads to elevated ______________ pressures and subsequent increased ________________ vascular pressure. If uncorrected, this may result in chronic pulmonary ____________________, _______________________ hypertrophy and ________________ heart failure. (Ch. 18- Alterations in Cardiac Function)

infection, papillary muscle

Regurgitation (insufficiency) may develop suddenly from valvular _____________ or rupture of a supporting ________________________. (Ch. 18- Alterations in Cardiac Function)

ATP, ions, ST-segment elevations

Reversibly injured cells have limited ________ supplies to power membrane pumps and therefore are predisposed to leakage of _________ across cell membranes-- this abnormal flux results in continuous flow, even when the heart is at *rest*, which leads to ______________________________ in ECGs. (Ch. 18- Alterations in Cardiac Function)

collagen, fibrinogen, adhesiveness, thrombus

Rupture of a plaque (in atherosclerosis) exposes an area composed of _____________ and other thrombogenic molecules. High _________________ level (smokers) and enhanced platelet ___________________ (hyperlipidemia) may enhance the risk of _____________ formation --> ischemia. (Ch. 18- Alterations in Cardiac Function)

subendothelial, aggregation, thrombus, enlarge

Rupture of an atherosclerotic plaque exposes ______________________ proteins and initiates platelet ___________________ and ______________ formation; components of this may be incorporated into the plaque, causing it to ____________. (Atherosclerotic plaque formation) (Ch. 18- Alterations in Cardiac Function)

chest pain, diaphoresis, breath, rest, nitroglycerin

Signs and symptoms of *myocardial infarction* include a severe crushing, excrutiating ________________ that may radiate to arm, shoulder, jaw, or back. Commonly associated by nausea, vomiting, ________________ (sweating), and shortness of __________. It lasts more than 15 minutes and is not relieved by _________ or _________________, like in classic/stable angina ** (Ch. 18- Alterations in Cardiac Function)

congestion, left atrium, pulmonary, SV

Signs/symptoms of *mitral stenosis* are due to _________________ of blood volume and increased pressure in the _______________ and _______________ circulation, as well as decreased _______ of the left ventricle b/c of deficient filling. (Ch. 18- Alterations in Cardiac Function)

ischemia, fibrillation, embolus, occlusion, vasospasm

Signs/symptoms of myocardial infarction are caused by: Prolonged or severe ______________, ventricular __________________, _____________, atherosclerotic _______________, prolonged ________________.*** (Ch. 18- Alterations in Cardiac Function)

insoluble, lipoproteins

Since cholesterol and triglycerides are ______________ in water, they are transported to and from tissue cells bound to small lipid-protein complexes called ___________________ (Ch. 18- Alterations in Cardiac Function)

NSTEMI

Some patients w/ ACS don't have ST elevation and instead have ST depression or T wave changes (w/ elevated serum markers)--- have _____________ ECGs; infarct size generally smaller and outcomes are better. (Ch. 18- Alterations in Cardiac Function)

stable angina pectoris

Stable plaques in atherosclerosis (CAD) are usually asymptomatic or may be associated w/ exercise-induced angina (_______________________________) (Ch. 18- Alterations in Cardiac Function)

hypertrophy

Stenosis progresses slowly over years to decades, which allows time for the affected heart chambers to compensate through myocardial cell __________________. (Ch. 18- Alterations in Cardiac Function)

pressure, resistance

Stenosis results in extra _____________ work for the heart b/c blood must be forced through high _________________ of narrow valve opening. (Ch. 18- Alterations in Cardiac Function)

cough, dyspnea, oxygenation, fatigue

Symptoms in *mitral stenosis* secondary to pulmonary congestion include: orthopnea, ____________, _____________ on exertion, paroxysmal noctura dyspnea, abnormal breath sounds, and poor arterial ___________________. Symptoms related to reduced left ventricular SV include ____________, poor activity tolerance, and weakness. (Ch. 18- Alterations in Cardiac Function)

thrombus, platelets

The initiating event in most MIs is development of a ______________ on top of an ulcerated or cracked atherosclerotic plaque (sudden change in structure). ______________ passing by the surface of ruptured plaque adhere to it, initiate formation of platelet plug, and activate clotting cascade. Resulting thrombus grows until it occludes the vessel and triggers transnmural MI. (Ch. 18- Alterations in Cardiac Function)

SV, afterload, high

The severity of *mitral regurgitation* (insufficieincy) is related to the amount of left ventricular ________ that is regurgitant, and depends, in part, on aortic resistance to flow (______________). A __________ (low/high) amount of this *increases* the amount of regurgitant flow. (Ch. 18- Alterations in Cardiac Function)

rate of coronary perfusion and myocardial workload

What are the 2 critical factors in meeting cellular demands for O2 that can lead to ischemia? (Ch. 18- Alterations in Cardiac Function)

atherosclerotic coronary arteries

What is the most common cause of cardiac ischemia? (Ch. 18- Alterations in Cardiac Function)

exertional dyspnea

What is the most common complaint in those w/ mitral stenosis? (Ch. 18- Alterations in Cardiac Function)

ischemic, myocardial infarction

When metabolic demand for oxygen exceeds supply, myocardium becomes ________________--> dysfunction in cardiac pumping and predisposes to abnormal heart rhythms. If this episode becomes severe/prolonged, irreversible damage to myocardial cells can lead to _____________________________. (Ch. 18- Alterations in Cardiac Function)

HDLs, liver

__________ are correlated w/ a *decreased* risk of atherosclerosis. They transport cholesterol from the peripheral tissues, back to the __________, thus removing atheromatous plaque. (Ch. 18- Alterations in Cardiac Function)

Ischemia

_______________ of cardiac cells occurs when oxygen supply is insufficient to meet metabolic demands. (Ch. 18- Alterations in Cardiac Function)

Atherosclerosis

_____________________ of coronary arteries is the source of nearly all coronary heart disease (coronary artery disease). causes progressive narrowing of arterial lumen and predisposes to processes that can precipiate MI (thrombus formation, coronary vasospasm, endothelial cell dysfunction) (Ch. 18- Alterations in Cardiac Function)

ST segment elevation (STEMI)

___________________________ on an ECG represents acute cellular injury and ischemia; shows that ischemic injury is ongoing. (Ch. 18- Alterations in Cardiac Function)

coronary heart disease (CHD)

also called *ischemic heart disease* and *coronary artery disease*; characterized by insufficient delivery of oxygenated blood to myocardium (ischemia) b/c of atherosclerotic coronary arteries (CAD) (Ch. 18- Alterations in Cardiac Function)

stenosis

failure of a valve to open completely (Ch. 18- Alterations in Cardiac Function)

mitral stenosis

flow of blood from left atrium into left ventricle impaired; characterized by abnormal left atrial-left ventricular pressure gradient during ventricular diastole when mitral valve is open (Ch. 18- Alterations in Cardiac Function)

angina pectoris

literally means "chest pain"; associated w/ intermittent myocardial ischemia and bouts of chest pain and associated symptoms generally recurrent and may be precipitated by conditions that increase myocardial O2 demand (exercise, stress, SNS activation, and increased preload, afterload, HR, or muscle mass) (Ch. 18- Alterations in Cardiac Function)

SA node

located in right atrium near superior vena cava inlet; receives innervation from sympathetic and parasympathetic branches of ANS; generally serves as the *pacemaker for the heart*, generating 70 action potentials per minute at rest.

triglycerides

major form of fat found in nature; primary function is to provide energy for the cell (Ch. 18- Alterations in Cardiac Function)

myocardial infarction

results when prolonged or total disruption of blood to myocardium causes cellular death by necrosis or apoptosis (Ch. 18- Alterations in Cardiac Function)

classic or stable angina

when onset of ischemia is predictable w/ certain activities and subsidsies w/ rest; patient has chronic coronary syndrome What type of angina is this? (Ch. 18- Alterations in Cardiac Function)