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Cardiac ConditionsCongenital 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 torest 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 notrelated, 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 inpulmonary 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, atheroscleroticcondition.

Progressive condition, not symptomatic until advanced state (when1/4 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 littleallowing 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 chestpain atrest, disnea (difficulty breathing), fatigue, anxiety,palpitations and light headedness.

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Hear click in the heart Regurgitation

Incomplete closure of valve (ie. Mitral)

Can be due to Rheumatic Heart Disease, stretching of papillarymuscles, 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

TreatmentEndocarditis 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 orperipheral 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)

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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 preventionValve 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 heartDisease (men below the age of 55, women b4 menopause), cigarettesmoking, 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 endothelialcells 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 cardiacarrest.

Coronary Heart DiseaseRisk Factors

1. High blood lipid level1. High cholesterol.1. High blood pressure

a. 140/90, but there are other stages1. Cigarette Smoking (tobacco)

a. If person quits after several years, lessons risk but still has risk.

1. Family history1. Diabetes1. Obesity1. 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.

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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) inlining of the muscle, usually in the ventricle.

Myocardial Infarction

Diagnoses ECG

Can show MI Blood Tests

http://www.healthcentral.com/animation/408/13/Heart_Attack.htmlhttp://www.healthcentral.com/animation/408/13/Heart_Attack.htmlhttp://www.healthcentral.com/animation/408/13/Heart_Attack.html

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CKMB (bradykin kinase), Troponin

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Heart Failure

Acute or Chronic

Right Sided

Left Sided

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AneurysmsAbdominal 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 ObstructionEdema

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