NPTE Cardiovascular and lymphatic PT

fibrous protective sac enclosing the heart

inner layer of pericardium

smooth lining of the inner surface and cavities of the heart

right A-V valve, anchored by chordae tendineae

leff A-V valve

pulmonary and aortic valves: prevent back flow

supplies atrium, R ventricle, infer wall of left ventricle, AV node, bundle of HIS, SA node

LAD: supplies the L ventricle and interventricular septum, apex

supplies the later and infer walls of L ventricle and portions of L atrium, SA node

goes straight to R atrium

SA node --> impulse spreads to both atria and they contract together-->stim the AV node --> transmits down the bundle of HIS to purkinje fibers --> impulse spreads thruout ventricles and contract together

conducting tissue of both ventricles; R and L branches of AV node; conducts the ventricles,

pacemaker of heart, initiates impulse; sympathetic and parasympathetic innervations affecting heart rate and strength of contraction

@ R atrium/ventricle junction; merges with bundle of HIS

amount of blood ejected with each HB. normal=55-100 mL/beat

amount of blood left in the ventricle at the end of diastole. Greater the filling, greater the blood pumped (Frank-Starling Law)

force the Left Ventricle must generate during systole to overcome aortic pressure to open the aortic valve

amount of blood discharged from the left or R ventricle per min (4-5L per min)

percentage of blood emptied from the ventricle during systole: clinically useful for measure of LV function

=SV / preload

normal = 60-70%, a lower EF = impaired

increased heart rate and heart dz

energy cost of myocardium

= HR*SBP

increases with activity and HR or BP

high pressure to low pressure

elasticiy of vessel walls, peripheral resistance, amount of blood in body

connect arteriols and venules

lymphatics, lymph fluid, lymph tissues, nodes, organs, (tonsils, nodes, spleen, thymus, thoarcic duct)

from capillaries to vessels to ducts to L subclavian vein

in medulla oblongata: cardioinhib center

• vagus nerve (CN X)
• slows heart rate and force of contraction
• causes coronary vasoconstriction

located in medulla oblongata: cardioacceleratory center

T1-T4 ganglia, releases epinenphern and nor-epinephrine

causes increase in rate and force of contraction

coronary vasodilation --> requires sympathetic inhibition

main mechanisms controlling heart rate

respond to changes in BP (circulatory reflex)

• sensitive to changes in blood chemicals (O2, CO2, lactic acid
• maintains pH

increased potassium ions, decreases the rate and force of contraction, produces EKG changes

decreased potassium ions

causes arrythmias, ventricular fib (V-fib)

increased calcium

increases heart actions

decreased calcium

depresses heart actions

viscosity of blood, diameter of arterioles/capillaries

increased blood volume and pressure

decreased arterial blood volume and pressure

• age (male >45, Female >55)
• family hx
• smoking hx
• sedentary
• obese
• HTN
• dyslipidemia
• pre-DM

washed out, absence of pink, rosy color

• 0 = absent pulses
• 1+ = pulse diminished
• 2+ = normal
• 3+ = full pulse, increased strength
• 4+ = bounding

supine, palpate 5th interspace, midclavical vert. line (APEX) of heart

60-100, <60 in athletic/trained

115-140 bpm

>100bpm

<60 bpm

variations in force and frequency

d/t arrythmias, myocarditis

d/t low SV or cardiogenic shock

d/t shortened ventricular systole and decreased peripheral presure; aortic insufficiency

aoric valve - 2nd right intercostal space at sternal border

pulmonic valve - 2nd left intercostal space @ sternal border

Tricuspid valve - 4th left intercostal space @ sternal border

mitral valve - 5th left intercostal space at midclavical

• S1 - (lub) normal closure of mitral and tricuspid valves -- marks beginning of systole
•    - decreased in 1st degree heart block

• S2 - (dub) normal closing of aortic and pulmonic valves, marks end of systole
•    - decreased in aortic stenosis

• 1. systolic - falls between S1 and S2
•    - indicates valvular dz or can be normal
• 2. Diastolic - falls between S2 and S1
•    - indicated valvular dz

• grade 1 - softest audible murmur
• grade 6 - audible with stethoscope off chest

Thrill - abnormal tremor with a murmur felt

• adventitious sound/murmur of arterial o venous origin
• common in carotid/femoral arteries

• abnormal heart rhythm with 3 sounds each cycle
•   1. S3 - ventric. filling, occurs soon after S2
•       
•     - indicative of congestive (LV) heart failure
•   2. S4 - assoc with ventric filling and atrial contraction; occurs before S1;
•     - indicative of pathology ie. coronary heart dz (CAD), MI, aortic stenosis, chronic HTN

12 leads

heart rate, rhythm, conduction, areas of ischemia and infarct, hypertrophy, electrolye imbalance

atrial depol

time required for impulse to travel from atria thru conduction cycle to purkinje fibers

ventricular depol

beginning of ventricular repol

time for electrical systole

count number of QRS complexes in a 6-second strip and multiple by 10

• pulse-less, emergency, adversely affects CO,
• requires CPR, medication, defib

chaotic activity of ventricle originating from multiple foci; unable to determine rate

EKG: bizzare/erratic activity without QRS complese

no effective CO, clinical death within 4-6 min

premature heartbeat arising from ventricle -- no p wave, a wide QRS that is premature, followed by long compensatory pause

Serious PVC = >6 PVC in min, paired, or in sequential runs

a run of 3 or more PVCs occuring sequentially; very rapid rate (150-200 bpm), may occur paroxsymally (abruptly); usually d/t ischemic ventricle - seriously compromised CO

wide/bizzare QRS, no P waves

atrial arrythmias, rapid, repetitive firing of one or more ectopic foci in the atria (outside sinus node)

P waves are abnormal or absent, rhythm is irregular, chronic or paroxsymal, rapid rate

CO is usually maintained

250-300 bpm

>300 bpm

140-250 bpm

if ventricular rate is slowed, CO is decreased

complete heart block, life threatening, requires meds and pace-maker

ischemia or injury - impaired coronary perfusion

can be up-slopping, down-slopping or horizontal

abnormal Q waves, ST elevation, T-wave inversion

increase HR

<120/<80

120-130/80-89

130-140/90-100

140-160/100-110

>160/>110

no known cause

D/t atherosclerosis, vascular d/o, renal dz, endocrine d/o, pregnancy, drug related

decrease in BP below normal, blood pressure not adequate for normal perfusion/oxygenation of tissues; may be related to bed rest, drugs, arrhythmias, blood loss/shock, MI

sudden drop in BP with change in position

• lightheadedness, dizziness, LOB
• drop in systolic more than 20mmHg or standing BP less than 100 should be reported and is significant

• Infant (<2 y/o) 106-110/59-63
• child (3-5 y/o) 113-116/67-74

• arterial pressure within the larger arteries over time, dependent upon mean blood flow and arterial compliance
• =[SBP+(DBP*2)]/3

• +1 = mild, noticeable to pt only
• +2 = mild, some difficulty, noticeable to observer
• +3 = moderate difficulty, but pt can continue
• +4 = severe difficulty, patient cannot continue

• New born = 30-40 bpm
• Adult = 12-20 bpm

increase in RR >22 bpm

decreased in RR to <10 bpm

increase in depth and rate of breathing

• DOE - brought on by exertion
• Orthopnea - unable to breathe when in reclined position (supine)
• paroxysmal nocturnal dyspnea (PND) - sudden inability to breathe occuring during sleep

(rales) rattling, bubbling sounds, d/t secretions in the lungs

whistling sounds

Normal = 95%-100%

abnormally low amount of O2 in the blood

low O2 level in the tissues

complete lack of O2

• 1+ = light, barely noticeable
• 2+ = moderate, bohtersome
• 3+ = severe, very uncomfortable
• 4+ = most severe pain ever experienced

diffuse, retrosternal pain, sensation of tightness, achiness, associated with sweating, dyspnea, indigestion, dizziness, syncope, and anxiety

sudden or gradual onset, occurs at rest or c activity, precipitated by physical or emotional factors, hot/cold temperatures,  relieved by rest or nitroglyerine

sudden onset, pain last for more than 30 min, may have no precipitating factors, not relieved by medications

cardiac pain can be referred to shoulders, arms, neck, or jaw

pain referred to back can occur from dissecting aortic aneurysm

• 1+ = mild, barely perceptible indentation <1/4 inch pitting
• 2+ = moderate, easily identified depression, returns to normal within 15 seconds, 1/4-1/2 inch pitting
• 3+ = severe, depression takes 15-30 seconds to rebound, 1/2-1inch pitting
• 4+ = very severe, depression lasts for >30 seconds or more, >1 inch pitting

dependent redness with PVD

curvature of the fingernails with soft tissue enlargement at base of nail

associated with chronic O2 deficiency, heart failure

pale, shiny skin, dry skin, loss of hair

abnormal pigmentation, ulceration, dermatitis, gangrene

tissues are thick, firm, and unyielding

dorsal skin of the toes and hands are resistant to lifting (lymphedema)

poor arterial perfusion

intermittent claudication with pain, cramping, and fatigue during exercise and relieved by rest

PaO2 - partial pressure of O2. based on the oxyhemoglobin desaturation curve

O2 below 90% in blood

low O2 levels in the tissues

complete lack of O2

shoulders, arms, neck, jaw

back

absent/diminished

curvature of the fingernails with soft tissue enlargement at base of nail -- associated with chronic O2 deficiency and heart failure

skin is thick, firm, unyielding, positive stemmers sign (lymphedema)

abnormal pigmentation, ulceration, dermatitis, gangrene

decrease in superficial skin temp

measure girth, pitting edema, caused by venous insufficiency or lymphedema, B edema = CHF

venous insufficiency can invalidate arterial tests

in standing - palpate one segment of the vein while tapping the vein 20 cm higher - if pulse wave felt in lower hand, valves are insufficient

in supine, elevate one leg for 1 min to 45 degrees, then place in dependent position, delayed filling (>15 s) is indicative of venous insufficiency

measuring systolic BP in non-palpable pulses for both venous and arterial insufficiency

• Scale:
• >1 = normal
• .8-1 = mild PAD
• .5-.8 = moderate PAD, intermittent claudication
• <.5 = severe PAD; ischemia of limb, rest pain

• insufficiency = pallor with elevation, rubor of dependency with dependent postion -- reactive hyperemia
• changes that take longer than 30s is indicative of PAD

exercise-induced pain or cramoing in the legs that is absent at rest - typically calf pain but can also occur in the butt hip thigh or foot

have pt ambulate until pain is felt, have pt sit and rest - note the time of walking. examine for numbness, coldness, pallor or loss of hair over tib anter

• palpate nodes = cervical, axilla, epitrochlear, superficial inguinal
• examine for edema - visual swelling, ROM, loss of funct mobility
• measure girth
• examine skin changes - texture, fibrotic changes
• presence of papules, leakage, wounds
• changes in function (ADL, funct mob, sleep)
• paresthesias?
• lymohangiography - x-ray of lymph nodes

reveal abnormalities of lung fluids, overall cardiac shape and size (cardiomegaly), aneurysm

• Dx and eval ischemic heart dz, MI
• identify myocardial blood flow, areas of stress induced ischemia (exercise test), old infarct
• thallium - injected into blood and will show up in normal tissue but not ischemic/infarct tissue -- can be used with exercise test

non-invasive; ultrasound to visualize internal structures - size of chambers, movement of valves, septum, abnormal wall movement

passage of tiny tube thru heart into blood vessels with contrast medium into coronary arteries and x-ray

provides info about anamtomy of the heart and great vessels, ventricular function, abnormal wall movements - allows determination of EF (eject fraction)

• into the R side of heart
• measures central venous pressure, pulm artery pressure, pulm capillary wedge pressure

elevation of CK or CPK (serum creatine kinase or creatine phosphokinase) - peaks at 24 hours; released after tissue injury

CK-MB (serum creatine kinase MB) - peaks at 12-24 hours; better isolates the source to the myocardium, high sensitivity

elevations in tropinin I, troponin T: high sensitivity 10 hours after injury

elevation of myoglobin

lipid panel - mg/dL -- used to determine coronary risk

Normal: SpO2 95%-100%; Clinical sig: SaO2 below 88% - supplemental O2 required

Normal: PaO2 80-100 mm HgClinical sig: increased in hypervent, decreas in cardiac decompensation, COPD, some NM d/o

• Normal: pH 7.35 - 7.45Clinical sig: <7.35 = acidotic, >7.45 is alkalotic increase in: -respitory alkalosis: hypervent, sepsis, liver dz, fever-metabolic alkalosis: vomiting, potassium depletion, diuretics, volume depletiondecrease in:-respiratory acidosis: COPD, respit depressants, myasthenia-metabolic
• acidosis (bicarbonate deficit): increased acids (DM, ETOH, starvation),
• renal failure, increased acid intake and loss of alkaline body fluids

Normal: PaCO2 35-45 mm HgClinical sig: increas in COPD; decreas in pregnancy, PE, and anxiety

• Normal: SpO2 95%-100%;
• Clinical sig: SaO2 below 88% - supplemental O2 required

• Normal: PaO2 80-100 mm Hg
• Clinical sig: increased in hypervent, decreas in cardiac decompensation, COPD, some NM d/o

• Normal: PaCO2 35-45 mm Hg
• Clinical sig: increas in COPD; decreas in pregnancy, PE, and anxiety

• Normal: pH 7.35 - 7.45
• Clinical sig: <7.35 = acidotic, >7.45 is alkalotic

• increase in:
• -respitory alkalosis: hypervent, sepsis, liver dz, fever
• -metabolic alkalosis: vomiting, potassium depletion, diuretics, volume depletion

• decrease in:
• -respiratory acidosis: COPD, respit depressants, myasthenia
• -metabolic acidosis (bicarbonate deficit): increased acids (DM, ETOH, starvation), renal failure, increased acid intake and loss of alkaline body fluids

• Normal: partial thromboplastin time (PTT) 25-40sec
• Clinical sig: increased in factor VII, IX, and X deficiency

• Normal: prothrombin time (PT) 11-15secClinical sig: increased in
• factor x deficiency, hemorrhagic dz, cirrhosis, hepatitis drugs
• (warfarin), if clotting time is 2.5 + more than normal, PT is contraind

• Normal: INR (international normalized ratio) - ratio of individual's PT to reference range 0.9-1.1
• Clinical sig:
• INR below 2=desirable
• INR above 2: consult with MD for increas risk of bleeding
• INR above 3 = risk of hemarthrosis

• Normal: bleeding time: 2-10 min; c-reactive protein CRP <10 mg/L
• Clinical sig: increased in platelet d/o, thrombocytopenia
• increased in levels associated with increased risk of athrosclerosis>100 mg/L associated with inflammation and infection

• Normal: prothrombin time (PT) 11-15sec
• Clinical sig: increased in factor x deficiency, hemorrhagic dz, cirrhosis, hepatitis drugs (warfarin), if clotting time is 2.5 + more than normal, PT is contraind

• Normal: partial thromboplastin time (PTT) 25-40sec
• Clinical sig: increased in factor VII, IX, and X deficiency

• Normal: INR (international normalized ratio) - ratio of individual's PT to reference range 0.9-1.1
• Clinical sig: INR below 2=desirable
• INR above 2: consult with MD for increas risk of bleeding
• INR above 3 = risk of hemarthrosis

• Normal: bleeding time: 2-10 min; c-reactive protein CRP <10 mg/L
• Clinical sig: increased in platelet d/o, thrombocytopenia
• increaed in levels associated with increased risk of athrosclerosis
• >100 mg/L associated with inflammation and infection

• Normal: WBC (white) 4,300 - 10,800
• Clinical sig: indicative of immune
• status; increased value in infection: bacterial and viral;
• inflammation, hematologic malignancy, leukemia, lymphoma, drugs
• (corticosteroids)
• decreased in aplastic anemia, B12 or folate deficiency with immunosuppression: increas risk of infect
• EXERCISE CONSIDERATIONS:
• - above 5000: light ex only
• - below 5000 with fever: exercise contraind
• - below 1000: use mask, standard precautions

• Normal: RBC (red):
• female 4.2-5.9 10^6/uL;
• male = 4.6-6.2 10^6/uL
• Clinical sig: increased = polycythemiadecreased = anemia

• Normal: ESR (erythrocyte sedimentation rate) -
• female=below 20 mm/hr;
• male = below 15 mm/hr
• Clinical sig: increased sedimentation rate in infection and inflammation:
• rheumatic or pelvic inflamm dz, osteomylitis used to monitor effects of
• tx; RA, SLE, Hodgkins dz

• Normal: Hct (hematocrit) % of RBC of the whole blood
• male = 45%-52%
• female= 37%-48%
• Clinical Sig: increased in erythrocytosis, dehydration, shockdecreased in severe anemias, acute hemorrhage
• EXERCISE CONSIDERATIONS:
• -more than 25% but less than normal = light ex only
• -less than 25% = exercise is contraind

• Normal: Hgb (hemoglobin)
• males: 13-18 g/dL
• females: 12-16 g/dL
• Clinical Sig: increased in polycythemia, dehydration, shock
• decreased in anemia, prolonged hemmhorage, RBC destruction (cancer or sickle cell dz)
• EXERCISE CONSIDERATIONS:
• - 8-10 g/dL: results in decreased ex tolderance, increased fatigue, and tachycardia; light ex only
• - below 8g/dL: ex contraind

• Normal: WBC (white) 4,300 - 10,800
• Clinical sig: indicative of immune status; increased value in infection: bacterial and viral; inflammation, hematologic malignancy, leukemia, lymphoma, drugs (corticosteroids)
• decreased in aplastic anemia, B12 or folate deficiency
• with immunosuppression: increas risk of infect
• EXERCISE CONSIDERATIONS:
• - above 5000: light ex only
• - below 5000: with fever, exercise contraind
• - below 1000: use mask, standard precautions

• Normal: RBC (red): female 4.2-5.9 10^6/uL; male = 4.6-6.2 10^6/uL
• Clinical sig: increased = polycythemia
• decreased = anemia

• Normal: ESR (erythrocyte sedimentation rate) - female=below 20 mm/hr; male = below 15 mm/hr
• Clinical sig:increased sedimentation rate in infection and inflammation: rheumatic or pelvic inflamm dz, osteomylitis used to monitor effects of tx; RA, SLE, Hodgkins dz

• Normal: Hct (hematocrit) % of RBC of the whole blood
• male = 45%-52%
• female= 37%-48%
• Clinical Sig: increased in erythrocytosis, dehydration, shock
• decreased in severe anemias, acute hemorrhage
• EXERCISE CONSIDERATIONS:
• -more than 25% but less than normal = light ex only
• -less than 25% = exercise is contraind

• Normal: Hgb (hemoglobin)
• males: 13-18 g/dL
• females: 12-16 g/dL
• Clinical Sig: increased in polycythemia, dehydration, shock
• decreased in anemia, prolonged hemmorage, RBC destruction (cancer or sickle cell dz)
• EXERCISE CONSIDERATIONS:
• - 8-10 g/dL: results in decreased ex tolderance, increased fatigue, and tachycardia; light ex only
• - below 8g/dL: ex contraind

• normal: 150,000-450,000 cells/mm^3
• clinical sig: increaesed in leukemia, hemoconcentration
• decreased in thrombocytopenia, acute leukemia, aplastic anemia, cancer chemo
• EXERCISE CONSIDERATIONS:
• - below 20,00: AROM, ADLs only
• - 20,000-30,000: light ex only
• - 30,000-50,000: moderate ex

• normal: 175-433 mg/dL
• clinical sig: increased in inflamm states, pregnancy, oral contracept
• decreased in cirrhosis, hereditary dz

• lipid plaques affecting moderate to large sized arteries
• thickening and narrowing of intimal layer of blood vessel wall from focal accumulation of lipids, platelets, monocytes, plaque, and other debris
• risk fx:
• -age, sex, race, familial hx of CAD
• - smoking, HTN, yperlipidemia, elevated cholestrol and LDL levels, elevated blood homocystine, emotional stress
• - obesity, sedentary lifestyle, DM, elevated fibrogen levels
• - 2 or more risk fx multiples the risk of CAD

• ranges from angina to infarction to sudden cardiac death
• imbalance of myocardial O2 supply and demand resulting in ischemic chest pain
• subacute occlusions may produce no symptoms
• symptoms present when lumen is at least 70% occluded

• chest pain or pressure due to ischemia, may be accompanied by levines sign (pt clenches fist over sternum)
• represents imbalance in myocardial O2 supply and demand;
• brought on by:
• 1. increased demands on heart: exertion, emo stress, smoking, extremes of temperature (cold), over eating, tachyarrhythmias
• 2. vasospasm: symptoms may be present at rest
• There are 3 types of angina:
• 1. stable: classica exertional angina occuring during ex or ativity; occurs at a predictable rate-pressure product, RPP (HRxBP), relieved with rest and/or nitroglycerin
• 2. unstable: (preinfarction, crescendo angina); coronary insufficiency at rest without any precipitating factors or exertion. chest pain increases in severity, frequency, and duration; refractory to treatment. increases risk for MI or lethal arrhythmia; pain is difficult to control
• 3. variant: (prinzmetal's angina): caused by vasospasm of coronary arteries in the absence of occulsive dz. responds well to nitroglycerin or calcium channel blocker long-term

• prolonged ischemia, injury, and death of an area of the myocardium caused by occlusion of one or more of the coronary arteries
• precipitating factors: atherosclerosis with thrombus formation, coronary vasospasm or embolism, cocaine toxicity
• zones of infarct:
• 1. central zone: consists of necrotic non-contractile tissue; electrically inert; on EKG - see pathological q-waves
• 2. zone of injury: area immed adjacent to central zone; non-contractile tissue, cells undergo metabolic changes, electrically unstable, EKG shows elevated ST segment in leads over damaged area
• 3. zone of ischmia: outer area, cells also under-going metabolic changes, electrically unstable, EKG shows T-wave inversion

• 1. transmural: q-wave infarct -- full thickness myocardium
• 2. nontransmural: (non-Q-wave infarct) -- subendocardial, subepicardial, intramural infarcts
• 3. sites of coronary artery occlusion: A. infer MI, R ventr infarct, distrubances of upper conduction system; R coronary artery; B. lateral MI, ventricular ectopy: circumflex artery; C. Anterior MI, distrubances of lower conduction system: left anterior descending artery
• impaired ventricular function results in:
• 1. decreased SV, CO, and EF
• 2. increased end diastolic ventricular pressure
• Electrical instability: arrythmias, present in injured and ischemic areas

• clinical syndrome in which the heart is unable to maintain adequate circulation of the blood to meet the metabolic demands of the body
• Types of heart failure:
• 1. left-sided heart failure: (CHF) characterized by pulmonary congestion, edema, low cardiac output due to backup of blood from L Ventricle to L atrium and lungs; occurs with insult to L ventricle from myocardial dz, excessive workload of the heart (HTN, valve dz, congenital defect), cardiac arrhythmias, heart damage.
• 2. right-sided heart failure: characterized by increased pressure load on right ventricle with higher pulm. vascular pressures; occurs with insult to R ventricle from LV failure, mitral valve dz, or chronic lung dz (cor pulmonale). produces hallmark signs of jugular vein distention and peripheral edema.
• 3. biventricular failure: severe LV pathology producing back-up in the lungs, increase PA pressure, and RV signs of HF
• Associated symptoms: Mm wasting, myopathies, osteoporosis
• clinical manifestations of heart failure
• compensated HF: heart returns to functional status with reduced CO and ex tolerance. Control achieved thru 1. physiological compensatory mechanisms; SNS stimulation, LV hypertrophy, anaerobic metabolism, cardiac dilation, aterial vasoconstriction and 2. medical therapy

• LV failure:
• S/S of pulm congestion: dyspnea, dry cough, orthopnea, paroxysmal nocturnal dyspnea, pulmonary rales/wheezing
• S/S of low CO: hypotension, tachycardia, lightheadedness, dizziness, cerebral hypoxia: irritability, restlessness, confusion, impaired memory, sleep disturbances; fatigue/weakness, poor ex tolerance, enlarged heart on chest x-ray, murmur(extra heart sounds), murmur of mitral or tricuspid regurgiation

• RV Failure:
• S/S of pulm congestion: dependent edema, wt gain, ascities, liver engorgement (heptomegaly)
• S/S of low CO: anorexia, nausea, bloating, cyanosis, R upper quadrant pain, jugular vein distension, cyanosis at nail beds, R sided S3 sounds, murmurs of pulm or tricuspid infficiency

• amount of O2 consumed at rest (sitting) = 3.5mL/kg per min
• MET levels: multiples of resting VO2; can be directly determined during ex tolerance tests (ETT) but not commonly done
• MET levels are estimated during ETT
• can be used to predict energy expenditure during certain activities

• Sternal precautions include:
• Do not lift more than 5-8 pounds.
• No pushing or pulling with your arms.
• Do not reach behind your back or reach both arms out to the side.
• Do not reach both arms above shoulder height.
• All for 6-8 wks post-surgery