Cardiac Disorders

• associated with aging
• Decreaes elasticity
• vessel wall becomes hard and thick
• lumen narrows

• associated with elevated reisk factor and a factor in many cases of CAD
• defpositys of lipid, cells, fibrin form and plague called an atheroma
• Lumen progressively narrows....ischemia
• Increases risk of PVD, MI, CVA

• Etiology: elevated cardiac risk factors also hypertension and use of oral contraceptives
• Diagnosis: erum lipid levels HDL lower than 35 LDL greater than 100
• Treatment: Diet control, Exercise, Weight Reduction, antigoaguland medications
• If advanced it may require surgery
• If not treated can reuld in stroke, ME or peripheral arterial disease

• Coronary Artery Bypass Graft (CABG)
• PTCA (balloon angioplasty)
• Stent
• Laser

• partial occlustion of the coronary arteries leads to ischmeia during times of high oxygen need
• An imbalance between o2 supply and demand
• Diffenrent Patterns: classic ecertional, Varlant (vasospasm), unstable

• Etiology: atherosclerosis vasospasm, myocaridal hypertrophy, severe anemia, respirtaory disease
• Precipitating Factors: exertion, stress, cold, large meal
• S&S: recurrent intermittent chest pain, may see pallor, diaphoresis, nausea. last for a nre seconds or minutes when the pt rest it goes away
• Treatment: Eliminate the triggering factor, Nitroglycerin

Exerice helps to reduce the risk factors but pt need to be monitored carefully

• Coronary Obsrtrucion leading to prolonged ischemia and cellular death
• Etiology: Thrombus builds up to completely occlude a coronary artery, vasospams and partial occlucion by atheroma, thrombus breaks free embolus travels to one of the coronary arteries

• inflammtiona - necrosis, area of necrosis is replaced by fibrous tissue (scar). scar is non contractile
• Enzymes are released which are helpful in making the diagnosis

• Severe chest pain that persists, LUE pain , neck, jaw, SOB, increased HR, weakness, sweaty, nausea
• rest and nitro have no effect

• EKG charnges: T wave inversion, ST elevation and abnormal Q
• Serum enzymes
• Further studies if need to know exten and prevent

• Complications: arrhythmia, cardiac arrest, death
• cardiogenic shouck wtih prolong period of decreased O2 to the brain
• CHF
• Treatment: thrombolytic mediation, administered within first hour
• Rest, O2 therapy, pain meds
• Anti-coagulant meds, other med to control cardiac function
• Then refer to cardic rehab

• Pt ed (pt is often very scared)
• Gradual return to exercise/activity in a monitored environment

SA- AV- Bundle Branches - Purkinje Fibers - contraction

damge to some aspect of the conduction system or sytemic cuase such as electolyte imbalance, high fever, hypoxia, stress, infection, drug toxicity (caffeine)

• Sinus node
• Atrial conduction
• AV node (heart blocks)
• Ventricular conduction

A rate of less than 60 beats per minute

A rate of greater than 100-160 beats per minute

Altering tachycardia/bradycardia

Extra contraction ectopic beats taht originate from an ectpic foci or teentry of an impulse that goes through damaged tissue

160-350 bmp

greater than 350bpm

• Conduction is excessively delayed or stopped athe the AV node or bundle of His
• Patrial block: 1st degree, prolonged PR 2nd degree periodic missed ventricular contraction
• Total Block: vetricales beat independent of the atria, very slow HR(30-45bpm), 3rd degree greatly reduced Do, fainting< may prdceed to cardiac arrest

• interference with conduction at one of the BB;s
• Wide QRS

fast ventriucle beats: can progress to v fib and cardiac arrest

• ectopic beats from the ventricle
• occasional PVC's are ok but when frequent or paired can proceed to V fib

• EKG, Holter monitor
• Treatment:
• Medication -antiarrhythmia meds
• Pacemaker- Temp or permanent

• Heart is unable to meet metabolic demands of the body
• Etiology: usually due to other problems: MI, valves, pulm disease ect
• Startes as a unilateral problem usually on the let but can progress to right side

• Fatigue
• Weakness
• Dizziness
• Dyspnea
• Exercise and cold intolerance

• Dyspnea (increase activity with breathing)
• Orthopnea (dificulty breathing in supine or when flat)
• Pulmonary edema
• rales, cough
• Easier to sleep with the head up

• Dependent edema
• Hepato and splenomegaly
• Ascites-abdominal distention with fluid
• Flushed face, distended veins
• Headache, vision problems

• xray: cardiomegaly, fluid in lugs
• ABG's: anoxia
• Arterial pressures: measured with catheters at specific locations

• Medical Management: treatment of the underlying coustes
• Implications for functional activites
• Monitor closely for signs of cardiac distress
• avoid excessive fatigues, stress, studden exertion
• Modify lifestyle, take meds

• Etiology: accompandies congenital heart defects
• Symptoms: feeding problems, decreased weight gain
• Decreased ability to sleep
• Cough rapid grunting respiration wheezing
• Treatment: Goal is to decrease workload on heart
• similar to adult treamtnet but need to be monitored closely as the grow( meds surguys supportive care)

• developmental defects that arises in the first 8 wks of gestation
• Etiology:
• multifactorial - influenced by genetic and prenateal environment
• Addociated with down syndrom, Fetal alcohol syndrome maternal diabetes
• Compensaion mechanisms: SNS kick in, HR increasesm, RR increases but this in ineffective over time

increased HR, DOE, tachypnea, clubbed fingers, exercise & cold intolerance

• Diagnosis: varies, Xray, cardiac cath, echo, EKG
• Treatment: Meds, surgery, Supportive care
• Therapy, NICU careful monitoring

Hole in the heart

• most common- aortic, pulmonay
• types- stenosis, incompetence, prolaspse

Combination of 4 defects: pulmonayr valve stenosis, ventricular septal defect, dextraposition of aorta, R ventricular hypertrophy

• follwing and infection antibodies form then react with connective tissue in the skin joints brain and heart. Set up infection & inflammation
• Pericarditis: inflammation of out layer, may include effusion
• Myocarditis: heart muslce may interfere wiht conduction
• Edocarditis: affects the valves, mostcommon problem with rheumatic fever, valves become edematous and develop vegetations affects heart function

• S&S: Low grade fever, leukocytosis, malaise, anorexia, fatigue, tachycardia, epistaxis, abdominal pain
• Diagnosis: Blood test anemis, decrease heart function tests, EKG changes
• Treatment: Antibiotics, future strep infection proptly treated, valve replacement
• Proohylactic peniceillin prio to invasive procedures

• Patho: organism envades the heart valves
• Organism causes inflammtion and formation of vegetation on the cusps
• Interfere with opening/ closing of the valves
• Pieces may break away forming emboli that cause infaction/ infarction of other tissues
• Etiology: predisposing factions: abnormal tieeus in the heart presence of microes inthe blood reduced host defenses

• S&S: heart murmur and other signs or impaired heart function
• Subacute: insidious onset, intermittent low grade fever/fatigue anorexia, splenomegaly, osler's nodes on fingers septic emboli from vegatations can cause additional problems CHF can develop in severe cases
• Acute: sudden marked onset with spiking fever chills drowsiness if heart valves are severely damages can reult in severe impairment of heart function
• Treatment: antibiotics for a minimum of 4 weeks otehr medicaiton to support hear function