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82 Cards in this Set
- Front
- Back
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What is the function of the CV system in gestation?
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Supply tissues with oxygen & essential nutrients AND remove waste products from tissue.
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What are the two systems of the adult heart?
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Right sided pulmonary circulation
Left sided systemic circulation |
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Where does the fetus get oxygenated blood?
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Mother via placenta
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Right-to-left shunt
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Divert non-oxygenated blood from pulmonary to systemic circulation.
REDUCES O2 sat of arterial blood |
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Left-to-right shunt
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Divert oxygenated blood from systemic to pulmonary circulation
Deprives systemic tissues of O2 |
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What type of shunt causes pulmonary hypertension?
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Left-to-right shunt
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Group of vascular disorders characterized by thickening & loss of elasticity of the arterial walls.
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Arteriosclerosis
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Atherosclerosis is characterized by what?
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Formation of atherosclerotic plaques in large & medium sized arteries.
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Major risk factors of atherosclerosis.
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Hyperlipidemia
Hypertension Smoking Diabetes Mellitus |
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Cholesterol is vital for synthesis of what, and how much of the body cholesterol is located intracellularly?
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Cellular membranes
Steroid hormones Bile acids 93% |
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Endogenous cholesterol is synthesized in the ______ and free fatty acids are derived from ______ ______.
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Liver
Adipose tissue |
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4 types of lipoproteins & what they transport.
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Chylomicrons - dietary triglycerides
Beta lipoproteins (LDL) - endogenous cholesterol Pre-beta lipoproteins (VLDL) - endogenously produced hepatic triglycerides to muscles & fat tissue Alpha lipoproteins (HDL) - endogenous extrahepatic cholesterol to liver |
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What is the major plasma cholesterol carrier?
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Beta lipoproteins (LDL)
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Receptor pathway clearance of LDL
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LDL -> Liver cell mb -> Liver cell -> bile
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Outside the liver, excess cholesterol is stored in the ____. ____ can extract this and transport it to the liver for excretion.
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Cytoplasm
HDL |
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Phagocytic pathway clearance of LDL
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Monocytes/macrophages have receptors for modified LDL and can clear 1/3 of plasma LDL.
Cannot regulate uptake and may become overstuffed (xanthomas) |
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Familial hyperlipidemias occur as a result of what?
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Inherited genetic defects
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What causes hypercholesterolemia and what are the major contributors?
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1. Dietary excess of cholesterol and/or genetic factors
2. Excessive caloric intake, excessive dietary cholesterol, & saturated fatty acids |
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What are the borderline & pathologic values for Total Serum Cholesterol?
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In middle aged adults (>40)
1. b/t 200 and 240 mg/dl 2. >240mg/dl |
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An increase in this blood level is an independent risk factor for atherosclerotic disease.
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Plasma total homocysteine level
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Deficiencies in what vitamins leads to an increase in homocysteine levels?
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Vitamin B12, B6, & folic acid
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Chlamydia pneumoniae & cytomegalovirus infections may increase risk for developing what condition?
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Atherosclerosis
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T/F
Chlamydia pneum. & cytomegalovirus are common infections, & require other factors to place individuals at risk for atherosclerosis. |
True.
These infect 50% of middle-aged adults & require environmental or genetic factors to place individuals at increased risk. |
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The atherogenic process is in response to what?
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Vascular endothelial damage
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Uncontrolled intracytoplasmic accumulation of LDL & VLDL will cause what?
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Cell death & rupture leading to formation of non-reversible of atherosclerotic plaques
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What are fatty streaks?
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Probably reversible lesions that may be precursors to adult plaques.
Appear as multiple, flat, yellow streaks on inner surface of vessels |
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Multifocal asymmetric elevations of the vessel lining with a firm, fibrous cap overlying a softer core of atheromatous & necrotic debris.
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Atherosclerotic plaques
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Where are atherosclerotic plaques most severe?
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Abdominal aorta
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Are "routine" or "complicated" plaques associated w/ thrombus formation, dystrophic calcification, hemorrhage into the plaque, or weakening of the vessel wall?
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"Complicated"
"Routine" plaques are precursors to "complicated" plaques. |
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Clinical symptoms of atherosclerosis are generally related to the hemodynamic effects on what parts of the body?
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Heart, brain, kidney, small bowel, and lower extremities
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Ischemic heart disease (IHD) is responsible for __% of total mortality in US & __% of deaths due to heart disease.
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30% & 75%
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Ischemic heart disease results from an imbalance b/t what?
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The availability of oxygen and the metabolic demand of the heart.
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The availability of oxygen to the heart may be affected by what 3 factors?
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Reduced coronary flow, increased metabolic demand, or decreased saturated hemoglobin availability.
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Acute IHD manifests as?
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Angina pectoris, acute myocardial infarction, & sudden cardiac death
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What causes angina pectoris?
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A temporary inability to supply sufficient oxygen to the heart muscles.
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How does nitroglycerin help with angina?
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It causes peripheral venous dilation, reducing blood return and workload on the heart.
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T/F
Angina is the result of atherosclerotic stenosis of the pulmonary arteries. |
False!
It is the result of stenosis of the coronary arteries. |
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Cause of 60% of the deaths related to ischemic heart disease
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Acute myocardial infarction
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T/F
In acute myocardial infarction, the myocardial injury is due to increased metabolic demand. |
False.
Myocardial injury is due to occluded or reduced blood flow, which may be caused by an occlusive thrombus developing of the surface of an atherosclerotic plaque. |
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The risk of acute thrombosis depends what?
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The biology of the plaque
--Gradually enlarging plaques will produce stable angina. --Acute thrombosis will cause an infarct. |
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What is the typical presentation of an acute myocardial infarction?
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Crushing, substernal chest pain unrelieved by rest or nitroglycerin, accompanied by nausea, vomiting, diaphoresis, arrhythmias, hypotension, shock
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Where do most infarcts occur?
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Distribution of the left anterior descending coronary arter
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During the first 24h after myocardial cell death what cytoplasmic enzyme is elevated?
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Serum CPK -- returns to normal in 3-5d
Serum LDH -- 7-12d |
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Which cardiac troponin is the most cardiac-specific?
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Troponin-I (cTn-I)
Begins to rise w/in 2hrs of myocardial cell injury & remains elevated for up to 2 weeks. May become preferred diagnostic marker. |
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What are the possible complications of acute myocardial infarction?
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arrhythmias (90%), L ventricular dysfunction, mural thrombosis -> embolism, rupture of L ventricle wall, & ventricular aneurysms
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What are the modes of intervention of acute myocardial infarction?
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Thrombolytic therapy, angioplasty, & coronary bypass
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How soon can sudden cardiac death occur after onset of symptoms?
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Less than 1 hour
Usually associated w/ fatal arrhythmias. 90% have severe coronary disease & 50% have evidence of old infarcts |
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What percentage of deaths from ischemic heart disease (IHD) are a result of chronic IHD?
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40%
Most patients have a hx of angina/MI and heart failure may follow a precipitating illness such as pneumonia. |
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What is valvular stenosis, and what does it cause?
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Failure of a valve to open.
Creates and obstruction to the forward flow of blood. |
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In acquired valvular stenosis, where is the primary abnormality almost always located?
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In the cusps or leaflets.
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What is valvular insufficiency?
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Inability of a valve to close properly causing a backward flow of blood.
Can be due to intrinsic valve disease or damage to supporting structures. Stenosis and insufficiency may coexist. |
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T/F Rheumatic heart disease is cardiac involvement in the systemic disease rheumatic fever?
T/F This affects children more than adults. |
True
True - 90% of first attacks occur b/t ages of 5 & 15 |
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Rheumatic fever causes pancarditis (inflamm. rx in all layers of the heart), what happens at each layer?
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Pericarditis - friction rub on auscultation due to acute fibrinous inflamm. of pericardium.
Myocarditis - cardiac arrhythmias due to focal necrosis & inflamm. Endocarditis - valvular stenosis & insufficiency from calcification of the leaflets/cusps of valves. **Most crippling & destructive part of the disease** |
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What are possible complications of rheumatic heart disease?
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First attack may result in severe damage to heart valves despite therapy & prophylaxis.
Cause of death may include cardiac failure, mural thrombosis & embolism, and bacterial endocarditis. |
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What do calcific aortic stenosis, rheumatic cardiac disease, mitral valve prolapse, and infective endocarditis have in common?
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They are all valvular diseases.
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What happens in calcific aortic stenosis?
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Calcified nodules develop & obstruct the flow of blood through the valve. Little to no fusion of cusps or leaflets.
--Usually seen in elderly patients and may be results of wear and tear valvular damage. |
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What is the survival rate for calcified aortic stenosis?
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2-3 years unless valve is replaced
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Mitral valve prolapse is a common condition that affects _-_% of the population (mainly _____) and may be _______ in origin.
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5-7%
young women congenital |
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What characterizes mitral valve prolapse?
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Enlarged mitral leaflets and/or elongated chordae (which may also enlarge and possibly fuse)
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Over time, what happens to patients with mitral valve prolapse?
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Most patients are asymptomatic, but death can occur from complications of infective endocarditis, chronic congestive heart failure, chordal rupture, or arrhythmia.
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What is infective endocarditis?
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The development of friable septic thrombi with embedded bacteria (vegetations) on heart valves or endocardial surfaces.
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What are the two clinical categories of infective endocarditis and what is the main difference between them?
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Acute endocarditis (ABE) & chronic endocarditis (SBE)
In ABE the thrombi contain virulent bacteria (i.e. Staph aurues), whereas in SBE the bacteria have a low virulence level (Staph viridans). |
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What populations are at risk for acute endocarditis (ABE)?
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IV drug users, chronic alcoholics, patients who have undergone previous cardiac surgery, or patients who have had foreign bodies introduced into the CV system.
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What are the symptoms of acute endocarditis (ABE)?
Subacute endocarditis (SBE)? |
ABE- Abrupt onset of fever, chills, and profound weakness. Embolic phenomena and cardiac decompression occur early.
SBE- Insidious onset with progressive weakness, weight loss, anemia, fever, occasional night sweats. |
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How do the mortality rates differ for acute and subacute endocarditis?
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ABE- 70% die from heart failure, emboli, arrhythmias, or uncontrolled sepsis.
SBE- 15% |
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Acute endocarditis affects the _____ valves, whereas subacture endocarditis affects the _____ valves.
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R-sided (pulmonary & tricuspid)
L-sided (aortic and bicuspid) |
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What is the second most common cause of cardiac failure and death?
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Hypertensive heart disease
*The 1st is ischemic heart disease. |
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Although most hypertension is of unknown etiology, what are two known causes of hypertension?
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Chronic renal disease and certain hormone producing tumors.
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What is the identifying hallmark of hypertension?
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Concentric hypertrophy of the L ventricle which thickens the wall, increases heart weight, and decreases the L ventricular volume.
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What happens when the heart is no longer able to adapt to the increase in work load due to hypertension?
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The heart begins to decompensate. The ventricle dilates (increasing heart size) and obscures the hypertrophic changes. This triggers symptoms of L sided heart failure.
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This refers to any inflammatory condition involving the myocardium.
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Myocarditis.
Ranges from fulminant disease w/ abrupt onset & acute cardiac failure to asymptomatic disease. |
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What populations are at greatest risk for myocarditis?
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Infants, pregnant women, and immunosuppressed patients.
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What are the clinical manifestations of myocarditis?
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tachycardia, arrhythmias, low grade fever, dyspnea, & malaise.
Inflammation usually resolves in 6-8 weeks but may progress to chronic disease requiring heart transplantation. |
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This term refers to non inflammatory disorders of the myocardium.
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Cardiomyopathy
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What differentiates primary cardiomyopathy from secondary cardiomyopathy?
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Whether the etiology is known (secondary) or unknown (primary).
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What are the three categories of cardiomyopathy?
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Dilated (congestive) cardiomyopathy, hypertrophic (obstructive) cardiomyopathy, and restrictive/infiltrative cardiomyopathy.
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Which type of cardiomyopathy may represent a common end point of a variety of previously undiagnosed cardiac diseases, can occur at any age, and is characterized by dilatation and hypertrophy of all chambers of the heart?
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Dilated (congestive) cardiomyopathy
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In which cardiomyopathy do the patients present with S&S of congestive heart failure and death is caused by progressive heart failure?
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Dilated (congestive) cardiomyopathy
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What are the two other names for hypertrophic (obstructive) cardiomyopathy?
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asymmetric septal hypertrophy (ASH) & idiopathic hypertrophic subaortic stenosis (IHSS)
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What type of cardiomyopathy is inherited and is characterized by dilated atria, disproportional hypertrophy of interventricular septum w/ myofiber disarray, decreased ventricular volume, mitral valve thickening, endocardial thickening of L ventricular outflow tract, and thickening of intramural arterioles?
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Hypertrophic (obstructive) cardiomyopathy
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In hypertrophic cardiomyopathy, if the septal hypertrophy is more prominent in the lower portion of the IVS, obstructive symptoms are ____ likely than if it were higher in the septal wall.
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Less
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What may happen to patients with hypertrophic cardiomyopathy that are unresponsive to medical therapy?
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They may develop arrhythmias or progressive heart failure complicated by embolization from atrial thrombi or infective endocarditis.
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