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cardio 1

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S&S of Cardiovascular Disease
pain
palpitations
fatigue
syncope
cough
cyanosis
peripheral edema
claudication
Pain
classical angina (chest pain of cardiac origin) with substernal chest pain
pressure, tightness, squeezing, heaviness
Palpitations
indicate underlying heart disease that is resulting in an abnormal heart rhythm (arrhythmia)
dyspnea
occur in response to activity
due to cardiac disease, pulmonary disease, deconditioning, etc
syncope
inadequate Q may lead to lightheadedness (fainting)
causes include: valvular dysfunction, arrhythmias, heart failure
cough
possible indicator of left sided heart failure with resulting back-up into the lungs (pulmonary congestion)
peripheral edema
in presence of congestive heart failure
claudication
leg pain
result of severe artherosclerotic disease affecting the arteries that supply the LEs
Disease Independent Changes due to aging
reduced number of myocytes and cells within the conduction system
development of cardiac fibrosis
reduced Ca++ transport across the membrane (muscle contractions)
reduced capillary density (aerobic performance)
reduced responsiveness to beta-adrenergic stimulation (decreased contractility, HR, and CO)
impaired autonomic reflex control of HR
age associated changes in the cardiovascular system
thickening of the left ventricular wall
stiffening/calcification of the ventricles, valves, and arteries
increased likelihood of clinically significant artherosclerotic heart disease
*non modifiable risk factor for heart disease*
functional changes in the cardiovascular system with aging
decrease in maximal HR
decrease in Q
decrease in VO2 max
increase in the incidence of arrhythmias
gender differences
Women:
increased incidence of mitral valve prolapse
increased in LV mass with aging
incrased risk of dangerous arrhythmias
decreased responsiveness to anticoagulants and thrombolytics (higher incidence of bleeding)
CAD in women
leading cause of death
risk of CAD rises sharply with menopause
hormonal influence
estrogen is cardioprotective
incrased HDL levels
reduces clotting risks
dilate blood vessels (maintain normal BP and blood flow)
pathogenesis of atherosclerosis theories
response to injury
monoclonal
lipid insudation
response to injury theory
damage to endothelial lining
platelets and monocytes adhere to injured area
platelets release PDGF promoting infiltration of smooth muscle cells from media to intima
plaque composed of smooth muscle cells, conn tiss, and cell debris form
lipids (LDL) deposited in the plaque
risk factors for CAD
non modifiable
age (83% > 65 years)
gender (m>f)
genetics (family history)
risk factors for CAD
modifiable
BP (SBP>140, DBP 90)
cholesterol (>200)
smoking
inactivity
obesity (BMI>30)
diabetes (fasting glucose level >126)
stress (type A)
emerging risk factors
C-reactive protein - marker for inflammation, elevated increase risk of MI
homosysteine - AA formed as body metabolizes methionine, elevated levels increase risk of MI, B vitamins can help moderate homocysteine levels
medical and surgical management of MI
treat symptoms (rest, O2, medications)
limit damage (meds, surgical intervention)
secondary prevention (lifestyle changes, meds, cardiac rehabilitation)
CABG- PT implications
sternal precautions:
no lifting, pulling, pushing for 6 weeks
log roll
no driving (4-8 wks)
ROM exercises (neck,s hldrs, torso)
scar mobilization
conservative if osteoporosis, diabetes, advnaced age
cardia rehab phases
I - inpatient phase
II- acute outpatient (up to 12 wks)
III- follows phase II (>6 months)
orthostatic hypotension
drop in SBP>20 and/or drop in DBP>10 with reflexive increase in HR (10-20%) as individual transitions from supine or sitting to a standing position
orthostatic hypotension causes
autonomic dysfunction
volume depletion
prolonged immobility
cenous pooling
meds
starvation/malnutrition
Myocarditis
inflammation of myocardium
usuallly result of viral or bacterial infection
causes: ischemic heart diease, radiation therapy, drugs, systemic lupus erythmatosus
cardiomyopathy
impaired ability of the cardiac muscle fibers to contract and relax
classifications: dilated (most common), hypertrophic, restrictive
risk factors for cardiomyopathy
radiation therapy
chemotherapeutic agents
rheumatic fever
alcohol abuse
sarcoidosis (different tissues/organs, pulmonary limitations)
obesity
HTN
smoking
CHD
anatomic defect in the heart that is present at birth
8 per 1000 babies
include symptoms of cyanosis and CHF
classified as cyanotic or acyanotic
Arrhythmias
irregular heart rhythm
myocardial ischemia, MI, CHF increase risk
range from benign to life threatening
Valvular Dysfunction
stenosis
regurgitation
prolapse
stenosisq
stiffening/calcification of valve
regurgitation
incompetent valve, allow retrograde blood flow
prolapse
MVP, valve leaflets billow back into the atrial chamber during systole and allow retrograde blood flow
pericarditis
inflammation of pericardium
idiopathic (85%), infections, MI, cardiac trauma (causes)
Aneurysm
abnormal stretching of the wall of an artery, vein, of the heart (diameter is 50% greater than normal)
risk increases with age
artherosclerosis is contributing risk factor for aneurysm develpment
treat surgically
rupture is catastrophic
PVD
pathologic conditions of blood vessesl supplying the extremities and major abdominal organs
classified as inflammatory, occlusive, vasomotor
affects LE>UE
artherosclerosis is a cause for PVD affecting LE, results in ischemic pain (claudication)
Acute MI
disruption of blood supply and ischemia to the myocardium with resulting necrosis and replacement of muscle fibers with scarring

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