Cardiac Conditions

Congenital Heart Disease

• Anatomic Defects
○ Children develop while forming in fetal development (wk 4-7), can see
during week 8.
○ Several reasons:
• Febrile illness (high fever)
• Lupus
• Diabetes
• Maternal Alcoholism
• Meds - Anti-convulsant meds, lithium.
• Hemodynamic Alterations
○ Abnormal shunting of blood from one side of heart to another.
○ Problem with heart going from fetal to outside of the womb circulation
○ Shunting from right to left side of heart or left to right side. (mixing of
blood)
• Status of Tissue Oxygenation
○ Cyanotic
• Right to left - Mixing of blood occurs, deoxygenated blood goes out to
rest of circ, therefore ppl b/c cyanotic.
○ Acyanotic
• Left to right - no cyanotic effect.
• Congenital Heart Disease
• Patent Ductus Arteriosus
○ Blood goes from RA to RV to Pulm artory directly to aorta
○ Premi babies take longer for duct to close
• Underdeveloped, also in SNS, might have to do with messages not
related, not pressures not being as they should be to close the gaps.
○ Can be seen on Xray
○ If does not close, can be repaired surgically, patch over ductus opening.
• Ventricular Septal Defect
○ Opening between both ventricles through septum.
○ Size determines severity.
○ Left side is higher pressure system than right, therefore oxygenated blood
in left ventricle shunts into right ventricle. Leads to increased size in
pulmonary artery and vein.
• Pulmonary hypertension and progressive cyanosis.
○ Quicker rate of blood returning to left atrium, less time for oxygenation,
more deoxygenated blood returning to left atrium - become cyanotic.
○ Echocardiogram - test used to determine where and size of opening.
○ Only surgically work on symptomatic individuals.
○ Can also use catheter, through femoral artery, attach/close the septum
(new)
• Can have more than one congenital heart defect.
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Valvular Heart Disease

○ Can occur on any valve in heart.
• Stenosis
○ Occurs on any valve
○ Aortic Stenosis
• Narrowing/thickening of valve leaflets, takes more blood pressure to
push through opening
• Most common in men, older people, high cholesterol, atherosclerotic
condition.
• Progressive condition, not symptomatic until advanced state (when
1/4 of usual size symptoms present:)
 Angina, syncope, symptoms of heart failure.
• Characteristic heart murmur, follow with echocardiograms also.
• Surgical - valve replacement (don't want to replace too early)
• Prolapse
• Ballooning back of valve leaflets, don't close nicely, can open a little
allowing some blood to regurgitate back through. (Big floppy valves)
• Can occur without regurgitation, but most people end up with
regurgitation.
○ Mitral Valve Prolapse
• Valve becomes fibrotic, usually asymptomatic, may have some chest
pain atrest, disnea (difficulty breathing), fatigue, anxiety,
palpitations and light headedness.
 • Hear click in the heart
○ Regurgitation
• Incomplete closure of valve (ie. Mitral)
• Can be due to Rheumatic Heart Disease, stretching of papillary
muscles, won't close effectively.
• Can be an acute cause, body not as able to tolerate.
• If occurs slower then body compensates, therefore can have
condition for years before symptoms present.
• Puts more pressure on side of the heart (left for mitral), affects stroke
volume and further pulmonary congestion. Longer process.
• Best to get to problem before symptoms present.
• Can surgically repair, decrease pressure in heart.

Rheumatic Heart Disease

• Due to complication with Rheumatic Fever
○ Caused by group A. Beta-hemolytic streptocaucus (iestrep throat,
pharyngeal) [not due to skin]
○ May cause interation between immune system and antigens from strep,
deposits in heart tissue - effects heart valves, veins, and SQ tissue.
○ Acute
• Strep throat
• Involvement of CT, necrosis in joints, heart valves.
• Further damage to these tissues - can cause permanent damage,
common cause of mitral stenosis.
• Treat with antibiotics
○ Chronic phase
• Rheumatic fever --> heart disease
• Use surgery to replace damaged heart valves.
• Beta Streptococcus
• Rheumatic Heart Disease
• Treatment

Endocarditis
○ Inflammatory process, infectious, inner layer of heart valve invaded by
bad acting bacteria on heart valves which destroy underlying tissue.
○ Already have heart disease.
○ See in Heart valve replacement patients, and other people with implants
in heart (opportunistic bacteria possible cause)
○ Staphylococcus, Strepcoccus, Enterococcus
○ Easily released and can travel through circ system --> cerebral circ or
peripheral circ.
○ Heart murmurs as vegetation grows.
• Subacute infective endocarditis
○ Don't appear as sick, develops over months, to an already damaged heart
valve.
○ Fever, signs of systemic infex
• Acute infective endocarditis (IE)
 ○ Occurs in heart valve that is previously normal.
○ See in IV drug users, introducing microorganisms into blood stream.
○ Become very sick, fever, signs of systemic infex.
• Antibiotic prevention

Valve Replacements
○ Determined by:
• Life expectancy
• Follow up care needed
• Metal Valves
○ Need a lot of follow up treatment, constant anti-coagulant therapy for life.
Last a long time.
○ Younger individual
○ Antibiotic therapy
• Tissue Valves
○ Pork!
○ Good for ten years.
○ Older person
○ Antibiotic therapy
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Coronary Heart Disease

• Atheroma
○ Plaque that forms.
• Atherosclerosis
○ Hardening of arteries
○ Develops from laying down of a fibro fatty lesion in the lining of a vessel.
○ See in large/medium sized arteries.
○ Begins as insidious (slow, hidden) process throughout life span, no
knowledge of occuring for years after.
○ Risk factors:
• High cholesterol, increased age, family history of Coronary heart
Disease (men below the age of 55, women b4 menopause), cigarette
smoking, obesity, HTN, diabetes, and more.
• Stable plaques
○ Stay there until mechanical trauma occurs (HTN, hemorrhage)
• Unstable Plaques
○ Caused by Endothelial injury, cause damage to inner lining of artery
• mechanical (high pressure), sends more platelets/monocytesto area,
lipids accumulate and form in smooth muscle cells or endothelial
cells until a plaque structure develops (smooth muscle cells,
macrophages, other leukocytes)
• Plaques sit for several years.
○ Body tries to heal area where damage occurs, more platelets and
macrophages forming a thrombus and an occlusion.
○ Give lipitor/statin drugs to stabilize plaques.
• Cardiac Arrest
○ Cessation of pumping of the heart can be caused by many reasons.
○ Versus MI - decreased O2 to certain area of heart, MI can lead to cardiac
arrest.

Coronary Heart Disease

Risk Factors
1. High blood lipid level
1. High cholesterol.
1. High blood pressure
a. 140/90, but there are other stages
1. Cigarette Smoking (tobacco)
a. If person quits after several years, lessons risk but still has risk.
1. Family history
1. Diabetes
1. Obesity
1. Secondary lifestyle (couch potatoes)
1. Alcohol

Myocardial Infarction (MI)

○ Imbalance b/t O2 supply and demand for its needs, severity determines
disease process, not severe --> agima, severe --> MI or sudden death.
 ○ Atherosclerosis most common cause (vessel over 50% occluded/blocked),
difficulty of cells to function.
• Ischemic Heart Disease
• http://www.healthcentral.com/animation/408/13/Heart_Attack.html
• Something sitting on chest, not everyone experiences in same way, mainly
men.
 Chest pain radiates up neck, down arm, up to jaw, to shoulders.
 Unrelenting nausea
 Diaphoretic (sweaty), pale
 Abnormal heart sounds, pericardial friction rub (inflammatory reaction in
potential space, hear rubbing sensation, painful)
• Women, can be chin, under bra line, under ear.
• Causes:
○ Sudden blockage of Coronary Artery
• No blood supply getting to myocardial tissue, will die if not relieved.
• 10 seconds before myocardial cells feel effects (cellular metabolism),
after afew minutes lose ability to contract, pumping function is
hampered, anaerobic process occurs, lactic acid builds up.
• Cardiac cells stay alive for 20 minutes without O2.
○ Hemorrhage into an atheromatous plaque
○ Arterial spasm
○ Sudden greatly increased myocardial oxygen requirements

Myocardial Infarction Complications

• Arrhythmias
○ Irregular heart rhythm due to damaged heart muscle, irregular signal.
○ Bradycardia (slower heart rate, heart block) in non lethal instances.
• Heart Failure
• Intracardial thrombi
○ In lining of the heart muscle --> decreased space for heart to fill,
decreased output.
• Pericarditis
○ Inflammation in potential space.
• Cardiac Rupture
○ Usually in septum (very lethal)
• Papillary Muscle Dysfunction
○ Ischemia over papillary muscles - impair closure, valves can be wide open.
• Ventricular Aneurysm
○ Aneurysm (thinning of the wall/vessel where blood accumulates
underneath, stretching wall/muscle until thins, can lead to rupture) in
lining of the muscle, usually in the ventricle.

Myocardial Infarction
• Diagnoses
○ ECG
• Can show MI
○ Blood Tests
 • CKMB (bradykin kinase), Troponin <-- peak after MI
• Treatments
○ Thrombolytics
• Giving streptikinase, some clot busters.
○ Coronary Angioplasty, PCI (percutaneous coronary angioplasty)
• See ballon angioplasty

Balloon Angioplasty

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• Angioplasty and a stent - run stent through catheter, blow stent to side of wall
to hold up against wall.

Other Treatments
1. ASA (Aspirin)
1. Lipid lowing drugs
a. Even is normal BP
1. Dietary Changes
a. Lower cholesterol, less sodium, leaner meat, more good fats, less
processed foods.
1. C-Reactive Protein
a. Blood test, predictor of future coronary events.
a. Marker of inflammation in body (chronic)
1. Homocysteine
a. Independent risk factor for development of Coronary disease.
a. May promote atherosclerotic plaques.
a. Often from dietary insufficiency of B6, B12, folate.

Angina
○ Inabil of coronary arteries to meet O2 demand.
○ Associated with fixed coronary obstruction.
○ Transient discomfort (3-5mins at a time) may be from lactic acid buildup.
○ Relieved with rest or nitrates.
○ Usually Substernal chest pain.
• Stable Angina
○ Narrowing of coronary arteries, not meeting metabolic needs of
pericardium, particularly after stressful activity (stairs).
○ Sit and rest, angina goes away.
• Prinzmetal Angina
○ Chest pain due to transient Ischemia, usually occurs in sleep REM cycle.
○ Caused by vasospasm of arteries, may or may not have athersclerotic
condition.
• No long term damage, but there is pain.
• Silent Ischemia
○ No pain, may be due to difference in SNS.
○ See in patients that had coronary artery bypass, and transplants.
• Mental stress-induced Ischemia
○ Increased heart rate, BP, increased Myocardial O2 demand that is not met.
○ Unknown whether mental stress leads to MI.
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Next Lecture

Hypertension
• Primary HTN
• Secondary HTN
• Isolated Systolic HTN
• Complicated HTN
• Malignant HTN

Hypotension
• Orthostatic (postural) Hypotension
○ Acute
○ Chronic
• Treatment

Cardiomyopathy
Types:
• Ischemic
• Restrictive
• Hypertrophic
• Dilated
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Heart Failure
• Acute or Chronic
• Right Sided
• Left Sided
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Aneurysms
Abdominal Aortic Aneurysm
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Veins
• Venous Insufficiency
• Varicose Veins

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 Embolism
• Fat
• Air
• Foreign Material

Arterial Thrombus
• Thrombus vs Embolism
• Arterial Thrombus
• Gangrene

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Edema
• Increased Capillary Permeability
• Low Plasma Proteins
• Increased Hydrostatic Pressure
• Lymph Obstruction

Edema
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