Diseases of the Cardiovascular System

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In what arteries of the body would an atherosclerotic complication cause the following conditions: stroke, aneurysm, peripheral vascular disease leading to claudication, heart attack or angina, and secondary hypertension.
- Stroke = cerebral arteries (e.g., the internal carotid and vertebrobasilar arteries that form the Circle of Willis);
- Aneurysm = thoracic aorta and abdominal aorta;
- Peripheral vascular disease = arteries of the lower extremities;
- Heart attack or angina = Coronary arteries;
- Secondary Hypertension = atherosclerosis of the renal arteries will activate the RAAS resulting in hypertension. However, primary hypertension is a complicated condition that we will cover later in this section.
Created through the degradation of IDL, has the highest concentration of cholesterol of all lipoproteins, carry cholesterol to cells throughout the body (receptor mediated) and is cleared by the liver.
A: Low density lipoprotein (LDL)
High levels of this inflammatory protein in the blood have become a major marker, along with high cholesterol, of atherosclerosis.
E: C-Reactive protein (CRP)
Made in the liver and carry triglycerides and cholesterol from the liver to adipose tissue and muscle—carries the highest amount of triglycerides of all the lipoproteins.
B: Very low density lipoprotein (VLDL)
Blocks platelet aggregation and activation of clotting factors and also blocks adherence of WBCs to endothelium—the "good" cholesterol.
D: High Density Lipoprotein (HDL)
As triglycerides are removed from VLDL, this lipoprotein is formed and is either taken up by the liver or remains in circulation where it is converted to low-density lipoprotein.
C: Intermediate lipoprotein (IDL)
Involved in the "Reverse cholesterol transport pathway" removing cholesterol from foam cells.
D: High Density Lipoprotein (HDL)
Are usually referred to as the "bad cholesterol" lipoprotein
A: Low density lipoprotein (LDL)
In this step, a rupture leads to instantaneous formation of a blood clot within the lumen of the blood vessel, stopping the flow of blood and leading to a heart attack or stroke.
D: Step 4:Complicated plaque with rupture of fibrous cap and hemorrhage.
This is the earliest form of the atherosclerotic lesion and consists of foam cells, T- cells, and smooth muscle cells.
B: Step 2:Fatty streak formation.
Neovascularization is an important contributor to plaque growth in this step.
D: Step 4:Complicated plaque with rupture of fibrous cap and hemorrhage.
LDL accumulates in the artery wall and undergoes chemical alterations and
becomes oxidized (O-LDL).
B: Step 2:Fatty streak formation.
In addition to the presence of foam cells and T-cells, smooth muscle cells migrate
and proliferate within the intima and begin to colonize the atherosclerotic plaque.
B: Step 2:Fatty streak formation.
O-LDL activates the endothelial cells to secrete chemokines causing the
monocytes to enter the intima and become mature macrophages.
B: Step 2:Fatty streak formation.
As a result of this the production of nitric oxide, the most potent endogenous
vasodilator as well as an inhibitor of inflammatory responses, is not produced.
A: Step 1:Endothelial dysfunction.
T-cells follow monocytes into the intima, secreting cytokines that activate
monocytes into macrophages.
B: Step 2:Fatty streak formation.
The central core of this plaque is covered by a fibrous cap that contains smooth
muscle cells and connective tissue components. These plaques can be either
stable of unstable.
C: Step 3:Formation of an atherosclerotic plaques.
Refers to atherosclerotic lesions that have undergone erosion, ulcerations,
fissuring of the surface, hemorrhage, thrombosis, calcification or weakening with aneurysm formation.
D: Step 4:Complicated plaque with rupture of fibrous cap and hemorrhage.
Differentiate between a "stable" and an "unstable" plaque in terms of lipid pools, thickness of fibrous cap, and vulnerability to rupture.
Stable fibrous caps have a small lipid core, thick cap, and may cause angina upon physical activity but is not ruptured prone and therefore less likely to cause a myocardial infarction. The opposite is true of an unstable plaque.
Having low levels of plasma LDL and high levels of HDL
Both low levels of LDL (i.e., genetics and diet) and high levels of HDL (either suggesting a male who exercise regularly or a female between puberty and menopause) would lower your risk.
Your gender and age
Males have higher risk than females between puberty and menopause (estrogen related). The process of atherosclerosis is progressing from adolescent (speed of
progression depended on genetics and lifestyle), so as we get older the risk
increases.
Having a parents that were active, kept a healthy body weight, but suffered from cardiovascular complications in their 50s.
This questions is based on the fact that atherosclerosis, like type 2 diabetes, is multifactorial. It sounds like these parents have provided some "bad genes" in terms of genetic threshold for the disease, but they have done their best to create an environment for their children to lower the environmental threshold and thus, the liability for heart disease.
Having normal blood pressure but a high fasting blood sugar
High blood pressure increases the risk for atherosclerosis, so having normal blood pressure is good. However, hyperglycemia (high fasting blood glucose) is one of the factors that initiate the first step in atherosclerosis, which is damage to the endothelial cells. A change is diet and activity level would be recommended.
Smoking because you have stressful job
Cigarette smoking is ranked among the leading risk factors in the etiology of atherosclerotic vascular disease. Smokers under stress commonly increase their consumption of tobacco. And overeating (and thus weight gain) is quite common in people under emotional stress. Cholesterol levels also tend to increase during periods of increased stress
Having low to normal levels of homocysteine
Hyperhomocysteinemia (elevated levels of homocysteine) is recognized in many studies as a strong, independent and casual risk factor for atherosclerosis. Therefore, having low to normal levels of homocysteine would reduce the risk of atherosclerosis.
Having a BMI over 30 and getting mad because you had to park so far away from Ahlberg Hall that you actually had to walk almost a quarter of a mile to attend classes.
Having a BMI over 30 would classify one as being obese. Obesity is a leading cause of preventable death, a growing epidemic, and a major contributor to cardiovascular disease risk and mortality in the U.S. Being upset about walking a moderate distance suggests a sedentary lifestyle which contributes to the risk of obesity.
Explain the following clinical processes and their purpose:
- 12-lead ECG stress test;
- Technetium Tc99m Sestamibi/Thallium-201 stress test;
- Coronary Angiography,
- Percutaneous transluminal coronary angioplasty;
- Coronary artery bypass graft.
12-Lead ECG Stress Test - -- The patient either walks on a treadmill or is given IV medication which simulates exercise while connected to an ECG machine.
- The patient begins at a very slow pace (1.7 mph) and low grade (0-10%) and speed and grade increases incrementally every 3 minutes until the patient shows positive signs (see below) or simply stops due to physical exhaustion. .
- Positive tests for CHD are ST elevations, ST depressions, and/or T wave
inversions which are usually accompanied by chest pains or shortness of breath.

Nuclear Scanning
Treadmill stress test similar to 12-lead ECG
radioactive isotopes (e.g., Thallium-201) are given IV and pictures of the heart are
taken using a gamma camera at rest and immediately following stress test
Areas of the heart that receive the radioactive substance and thus sufficient blood
flow will "glow" whereas the area of the heart not receiving blood will be "dark".
Rest pictures are compared to exercise pictures to determine extent of coronary
arterial blockage.

Coronary Angiograph
A catheter is inserted into the femoral artery (i.e., groin area) or arm.
The tip of the tube is positioned in both the right and left coronary arteries and contrast medium or dye is injected.
X-ray pictures are obtained to identify areas of significant blockage.

Percutaneous Transluminal Coronary Angioplasty (PTCA)
Balloon tip catheter with drug-eluting stent is introduced into the atherosclerotic lesion of the coronary artery
Balloon tip is inflated, opening artery and pressing the stent into the wall of the artery
Balloon tip is deflated and removed leaving stent in place.

Coronary Artery Bypass Graft (CABG)
- Median sternoptomy is performed and catheters introduced to right atrium and arch of aorta and connected to heart lung machine
- heart is stopped by cardioplegia
- graphs using saphenous vein, radial artery, and/or internal mammary artery are used to form an anastomosis beyond coronary lesion
- minimally invasive heart surgery using "The Port Access Techniques" where
heart lung machine and cardioplegia are also being used.
Compare the technique of Totally Endoscopic Coronary Artery Bypass Surgery (TECAB) to Coronary Artery Bypass Graft (CABG).
- eliminates the need for a large (6-10 inch) incision made down the sternum (breastbone) to access the heart, which reduces a patient's surgical trauma;
- Less pain (and need for pain medication)
- Less scarring
- Shorter hospital stay
- Quicker recovery and return to normal activities, and even light sports, within two to three weeks after the intervention
What are the components of blood pressure? Which component controls systolic blood pressure? Diastolic blood pressure?
See pic
When considering hypertension, what is meant by "end organ damage"? Give examples.
End organ damage results from chronic (long duration) high blood pressure and includes heart failure due to ventricular hypertrophy, cerebral arterial disease (causing stroke), damage to vessels of the retina (retinopathy), peripheral vascular disease, and damage to the kidneys (hypertensive nephropathy) resulting in kidney failure.
If an individual has a blood pressure of 140/80, what is their pulse pressure? Would that be considered a "healthy" pulse pressure (ie., what is the "cut off").
140 - 80 = 60 pulse pressure; Healthy pulse pressure <60 mm Hg
In systolic Hypertension of the elderly, what characteristics within the aorta causes high levels of systole? Low levels of diastole? What is the best predictor of complications due to systolic hypertension the elderly.
- The aorta and its major branches becomes thickened and the collagen and elastic in the tunica adventitia and media become "brittle" with the wear and tear of life. As a result, these vessels become less compliant;
- The stiff vessel walls during diastole results in less diastolic recoil. Recall that diastolic recoil of large arteries plays a role in diastolic pressure;
- Pulse pressure is a better predictor of end-stage renal disease, cerebro-and cardio- vascular events in the elderly.
What follow-up should be done to determine if white coat high blood pressure is in fact, hypertension?
Monitoring the blood pressure at home by blood pressure cuff or continuous monitoring equipment or at a local pharmacy or grocery store with a blood pressure machine can help estimate the frequency and consistency of higher blood pressure readings.
What is borderline hypertension? What should be done about it?
Borderline hypertension is defined as mildly elevated blood pressure that is found to be higher than 140/90 mm Hg at some times and lower than that at other times. People with borderline hypertension should have continued follow-up of their blood pressure and monitoring for the complications of hypertension.
No identifiable etiology, accounts for 95% of hypertension.
A: Primary hypertension
Main causes are chronic renal failure, renal arterial stenosis, and
pheochromocytoma.
B: Secondary hypertension
The cause is multifactorial (i.e., polygenic and environment) and onset typically
in 40's and 50's.
A: Primary hypertension
The association between alcohol and high blood pressure is particularly noticeable when the alcohol intake exceeds how many drinks a day?
Five (5) drinks a day.
Increases peripheral resistance by increasing blood vessel length
C: Obesity
Has a synergistic effect on aortic stiffness and, therefore, blood pressure.
A: Coffee and smoking
Any food packaged or canned has a high prevalence of this hypertensive related
substance.
B: Salt
Secretion of inflammatory mediators causes endothelial dysfunction resulting in
an increase in peripheral resistance due to arterial stiffness and vasoconstriction.
C: Obesity
Increases blood pressure by activation of the renin-angiotensin-aldosterone-
system (RAAS).
C: Obesity
To have a positive effect on reducing hypertension, what should be the intensity, time (in minutes), and the frequency (days per week) one should perform aerobic exercise?
To reduce blood pressure it is prescribed to perform brisk walking (or any aerobic exercise at a moderate to hard level of exertion) for 30 or more minutes for at least 5 days per week.
What are the two main factors that increase the risk of an aneurysm?
Atherosclerosis and hypertension
When addressing the issue of symptoms, what is a similarity between a cerebral
and aortic aneurysm?
Both usually cause no symptoms until they rupture.
In what anatomical location (ascending, arch, thoracic, abdominal) does an aortic
aneurysm usually form?
Abdominal aorta.
In terms of the three layers of the aorta, differentiate between at "true" aneurysm
and dissecting aneurysm. In which does a false channel develop?
A "true" aneurysm involves all three layers. In a dissecting aneurysm, the inner lining of the aortic wall tears and blood surges through the tear, separating (dissecting) the middle layers from the outer layer of the wall. As a result, a new, false channel forms in the wall.
In treating abdominal aortic aneurysm, what treatment might be given during
watchful waiting and why?
In watchful waiting , the patient will usually have regular CT scans or ultrasounds to watch the aneurysm. If the patient has high blood pressure, blood pressure medication will be given to lower the pressure on the weakened area of the aneurysm in an attempt to slow the progression of the aneurysm.
What are the advantages of an endovascular stent graph over open abdominal
surgery graph repair? Disadvantage?
Endovascular stent graph therapy has the advantage of avoiding abdominal surgery, aortic clamping, and minimize blood loss, resulting in shorter intensive care and hospital days.
One third of patients receiving endovascular stent graph therapy may require secondary procedures to maintain device patency or to treat endoleak.
What is the only treatment for thromboangiitis obliterans?
Smoking cessation.
Go through the three phases of Raynaud's phenomenon and explain changes in
color of the digits to what is occurring in the vasculature of the digits.
- Skin of the digit will appear pale as a consequence of absent cutaneous flow due to vasoconstriction of the digital arteries/arterioles;
- The second phase is the cyanotic phase in that the digits may appear blue to purple caused by deoxygenated blood in the capillary beds of the fingers;
- The final phase is a post ischemic hyperemic phase in which increased blood flow to the skin causes a blushed appearance.
What are the demographics of persons with primary Raynaud's phenomenon?
More women than men are affected, and approximately 75 percent of all cases are diagnosed in women who are between 15 and 40 years old.
Define Secondary Raynaud's phenomenon.What two condition commonly cause
secondary Raynaud's phenomenon?
- Patients have an underlying disease or condition that causes Raynaud's phenomenon;
- Scleroderma and systemic lupus erythematosus.
Is there a known cause of varicose veins? Is the problem with varicose veins--
the valve or the vessels wall?
- There is no known cause of varicose veins, but it is thought that the weakness of venous walls is inherited;
- The main problem is theweakness of the venous walls which, over time, stretch and become longer and wider, causing the valve cusp to separate, allowing backward flow into the superficial veins.
Which of the following is NOT a symptom of varicose veins?
a. Aching, painful legs (stretching of vein walls and accumulation of metabolites);
b. Ischemia to the lower extremities;
c. A feeling of heaviness, tiredness, and aching (edema and metabolites);
d. Persistent itching of the skin over the affected area (scratching may causes
secondary skin infection);
e. Changes in skin color (Stasis pigmentation):
B; A bit of a "tricky" question. Ischemia is a restriction in "arterial" blood supply to tissues, causing a shortage of oxygen and glucose. The symptoms of varicose veins are due to venous stasis. However, long standing varicose veins can cause capillary pressure in the tissues to increase, thus restricting the inflow of arterial blood.
If not treated, varicose veins could lead to what complications? Can varicose veins be cured?
- Phlebitis as well as dermatitis that could progress to a decubitus ulcer.
- Varicose veins cannot be cured and relies on the different forms of treatment to relieve the symptoms, improve appearance, and prevent complications
Laser Therapy (Pulsed Light) treatments
C: Non-surgery
Endovenous laser treatment
B: Surgery
Elevating the legs—by lying down or using a footstool when sitting.
A: Conservative
Stripping of the saphenous vein
B: Surgery
Injection Therapy (Sclerotherapy)
C: Non-surgery
Elastic stockings (support hose) that compress the veins and prevent them from
stretching and hurting.
A: Conservative
Why is pericarditis considered a "secondary condition"?
Pericarditis is often secondary to other disorders such as infection (bacterial, viral, fungal, rickettsia); trauma of surgery, especially open heart surgery; neoplasm; metabolic conditions (uremia due to kidney failure), and/or immunologic conditions (eg., systemic lupus eryhematosus).
Sufficient accumulation of fluid in the pericardial cavity that significantly limits the venous return to the heart.
C: Cardiac tamponade
Fibrous scaring with occasional calcification of the pericardium causing the visceral and parietal pericardial layers to adhere, obliterating the pericardial cavity.
E: Constrictive pericarditis
Management of cardiac tamponade.
D: Substernal transdiaphragmatic aspiration
Use of a stethoscope can identify a pericardial friction rub.
A: Acute pericarditis
The presence of exudate in the pericardial cavity that usually does not produce
symptoms.
B: Pericardial effusion
The definitive treatment for this condition is pericardial stripping.
E: Constrictive pericarditis
Results in a fibrotic lesions encasing the heart in a rigid shell, reducing filling
volume or preload and therefore, cardiac output.
E: Constrictive pericarditis
Involves a sudden onset of chest pain that worsens with respiratory movements
and may be confused with acute myocardial ischemia.
A: Acute pericarditis
Can be caused by amyloidosis or hemochromoatosis.
C: Restrictive cardiomyopathy
Also called "congestive cardiomyopathy".
A: Dilated cardiomyopathy
The walls of the heart, especially the septum, are significantly thicker than
normal and this thickness prevents the ventricles from relaxing between beats.
B: Hypertrophic cardiomyopathy
While the rhythm and pumping action of the heart is normal, the stiff walls of the ventricles keep them from filling normally, restricting preload and therefore, restricting stroke volume
C: Restrictive cardiomyopathy
Weakened, enlarged heart chamber that restricts cardiac output and the person's ability to perform activity of daily living.
A: Dilated cardiomyopathy
Peripartum cardiomyopathy.
A: Dilated cardiomyopathy
Although there is a genetic predisposition for this condition, other causes could
toxic (alcohol), metabolic (hyperthyroid), or infection (viral myocarditis).
A: Dilated cardiomyopathy
In some instances, the septum bulges into the lower left chamber restricting aortic
outflow and causing mitral regurgitation.
B: Hypertrophic cardiomyopathy
Echocardiogram will show grossly dilated left ventricle, severe hypokinesia and
rotary motion rather than contractile motion.
A: Dilated cardiomyopathy
Dyspnea while lying in a prone position.
B: Orthopnea
Attacks of sever shortness of breath or coughing occurring at night and awakening
the person.
C: Paroxymal nocturnal dyspnea
Shortness of breath on exertion
A: Dyspena
Allows leakage of blood from the left ventricle and into the left atrium during ventricular systole.
D: Mitral valve regurgitation/insufficiency
Is the most common form of valvular heart disease it can be caused by a papillary muscle rupture of dysfunction.
D: Mitral valve regurgitation/insufficiency
Will cause an enlarge left ventricle due to the increased pressure gradient.
A: Aortic valve stenosis
Greater than 50% of this valvular heart disease is caused by calcification of the
valves with age.
A: Aortic valve stenosis
Will cause a left atrial pressure of to rise from 5 mmHg to about 20-25 mmHg.
C: Mitral stenosis
Will increase pulmonary capillary pressure resulting in pulmonary edema.
C: Mitral stenosis
This valvular heart disease will cause blood to flow from the aorta into the left
ventricle during ventricular diastole.
B: Aortic insufficiency/regurgitation
For this course, what are the two main causes of valvular heart disease?
Rheumatic heart disease and infective endocarditis.
What causes Rheumatic heart disease? Explain the immunologic aspects of this disease.
- Rheumatic fever develops in children and adolescents following pharyngitis with group A beta-hemolytic Streptococcus (ie, Streptococcus pyogenes);
- In 1-3% of those in whom the pharyngeal streptococcus infection occurs, they will make antibodies that cross react with cardiac tissue, activating the complement system, and causing inflammatory destruction.
Why is the term "pancarditis" associated with rheumatic heart disease? What are
Aschoff bodies?
- "Pancarditis" means that all three layers of the heart are involved: endocardium (valvular heart disease); myocardium (Aschoff bodies); and pericardium (pericarditis);
- Aschoff bodies are inflammatory areas of the myocardium
What are the three processes involve in the pathogenesis of infective
endocarditis?
- the endocardium (ie., heart valve) must be "prepared" usually by endothelial damage (eg., rheumatic heart disease, artificial [prosthetic] heart valve, history of previous endocarditis, or congenital heart/heart valve defects) in order for microorganisms to colonize the valve;
- blood-born microorganisms (eg., streptococci) must adhere to the damaged endocardial surface;
- an adherent microorganism must proliferate (ie, grow on the valve).
A person has an EDV of 150 ml and an ESV of 50 ml, what is this person's SV? What would be the ejection fraction (Ef)? Would this person's Ef be considered normal?
- SV = 150-50 = 100 ml
- Ef = SV/EDV = 100/150 = .66%
- Yes, ejection fraction of 55-75% is considered normal.
If the person discussed in the last question had an ESV of 100, what would be the Ef? What this Ef suggest in terms of level of heart failure?
- SV = 150 - 100 = 50 ml; Ef = 50/150 = 33%
- This person not only is in heart failure but is also at risk of life threatening irregular beats causing cardiac arrest
What is the forward affect of right heart failure? Left heart failure?
The forward affect of both right and left heart failure is reduced cardiac output and, therefore, low blood pressure. Overall affect of low blood pressure is to activate the Renin-Angtiotensin-Aldosterone System (RAAS)
What is the backward affect of left heart failure? Name four symptoms.
- Pulmonary edema
- Dyspnea during light activity and at rest; rales; chronic cough; "hunger" for air.
What is the backward affect of right heart failure? What is ascites?
- Increased volume and pressure in the great veins causing jugular vein distension; Increased volume in distensible organs (hepatomegaly, splenomegally); Hepatomegaly can lead to ascites; and Peripheral, dependent edema in feet and ankles.
- Accumulation of fluids in the abdominal cavity.
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