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Flashcards in Cardiovascular diseases and cardiac rehab Deck (77)


disease of lipid laden plaques (lesions) affecting moderate and large size arteries

thickening and narrowing of the intimal layer of the blood vessel wall from focal accumulation of lipids, platelets, monocytes, plaque and other debris

part of CAD that leads to ischemia to the myocardium that can progress to injury and/or death


acute coronary syndrome (ACS)/ Coronary artery disease (CAD)

arthersclerotic disease; ranges from angina to infarction to sudden cardiac death
-leading cause of death in US

imbalance of myocardial oxygen supply and demand resulting in ischemic chest pain

symptoms present when lumen is 70% occluded

3 common presentations but may also have silent ischemia diagnosed by presence of a new pathologic Q wave
-most common in patients with diabetes, patients may have ischemia without any symptoms
-subacute occlusions may also produce no symptoms

1- angina
3-heart failure
4-sudden death, usually due to significant ischemia or ventricular arrhythmia


angina pectoris

chest pain or pressure due to ischemia; may be accompanied by Levine's sign- clenches fist over sternum

represents imbalance in myocardial oxygen supply and demand; brought on by:
-increased demands on heart: exertion, emotional stress, smoking, extremes of temperature (*cold), overeating, tachyarrhythmias
-vasospasm- may be present at rest

women more often describe sensations of discomfort, crushing, pressing and bad ache when referring to angina

with angina, patients often describe SOB, fatigue, diaphoresis and weakness as symptoms of ACS

older adults present more often with atypical symptoms (absence of chest pain): dyspnea, diaphoresis, nausea and vomiting and syncope


types of angina

1- stable:
-classic exertion angina occurring during exercise
-occurs at a predictable RPP
-relieved with rest and/or nitroglycerin

2-unstable (preinfarction, crescendo angina)
-coronary insufficiency at any time w/out 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 occlusve disease
-responds well to nitroglycerin or calcium channel blocker long term


myocardial infarction

prolonged ischemia, injury and death of an area of the myocardium caused by occlusion of one or more of the coronary arteries

precipitating factors:
-atherosclerotic heart disease with thrombus formation
-coronary vasospasm or embolism
-cocaine use

Impaired ventricular function results in:
-decreased SV, CO and EF
-increased EDVP

electrical instability: arrhythmias, present in injured and ischemic areas


zones of infarction

zone of infarction:
-consists of necrotic, non contractile tissue
-electrically inert
-ECG: pathological Q waves

zone of injury:
-area immediately adjacent to central zone
-tissue is non contractile
-cells undergoing metabolic changes
-electronically unstable
-ECG: elevated ST segments in leads over injured area

zone of ischemia:
-outer area
-cells also undergoing metabolic changes
-electrically unstable
-ECG: T wave inversion


sites of coronary artery occlusion

R coronary A:
-inferior MI, RA, RV infarction, disturbances of upper conduction system
-blockage could result in arrhythmias, which can be fatal

L coronary A:
-supplies anterior, superior and lateral walls of the LV and the inter ventricular septum
-blockage usually causes LV failure, which leads to pulmonary edema

Circumflex A:
-lateral MI
-ventricular ectopy

L anterior descending A:
-anterior MI
-disturbances of lower conduction system


heart failure

clinical syndrome in which the heart is unable to maintain adequate circulation of the blood to meet the metabolic needs of the body

1- L sided heart failure
2- R sided heart failure
3-Biventricular failure
4- compensated heart failure

associated symptoms:
-muscle wasting

-decreased CO
-elevated end diastolic pressures (preload)
-contractile deficiency (decreased SV and contractile force)
-impaired ventricular function


Left sided heart failure

(congestive heart failure, CHF)

characterized by pulmonary congestion, edema and low CO due to backup of blood from the LV to the LA and lungs.

occurs with:
-insult to the LV from myocardial disease
-excessive workload of the heart (HTN, valvular disease or congenital defects)
-cardiac arrhythmias or heart damage

S&S of pulmonary congestion
-dyspnea, dry cough
-paroxysmal nocturnal dyspnea
-pulmonary rales, wheezing

S&S of low CO:
-cerebral hypoxia: irritability, restless, confusion, impaired memory, sleep disturbances
-fatigue, weakness
-poor exercise tolerance
-enlarged heart on chest x-ray
-S3 heart sound, possible S4
-murmurs of mitral or tricuspid regurgitation


Right sided heart failure

reduced venous return to the heart from the systemic circulation due to failure of RV; increased pulmonary artery pressures with peripheral edema

characterized by:
-increased pressure load on the RV with higher pulmonary vascular pressures
-mitral valve disease, or chronic lung disease (cor pulmonale)
-produces hallmark signs of jugular vein distention and peripheral edema

-dependent edema
-weight gain
-ascites (abnormal abdominal fluid retention)
-liver engorgement (hepatomegaly)

-anorexia, nausea, bloating
-R upper quadrant pain
-jugular vein distension
-R sided S3 heart sounds
-murmurs of pulmonary or tricuspid insufficiency


Biventricular failure

severe LV pathology producing back up into the lungs, increased PA pressure and RV signs of HF


compensated heart failure

heart returns to functional status with reduced CO and exercise tolerance

control is achieved through:
-physiological compensatory mechanisms: SNS stimulation, LV hypertrophy, anaerobic metabolism, cardiac dilatation, arterial vasoconstriction
-medial therapy


cor pulmonale

failure or hypertrophy of RV resulting from disorders of the lungs, pulmonary vessels or chest wall

the lung pathology (chronic bronchitis or emphysema) produces pulmonary artery HTN that creates a problem for the RV

usually chronic, but may be acute and reversible


treatment for heart CHF

bed rest
sodium restriction
measures to improve myocardial contractility and correction of arrhythmias

1-Digitalis (digoxin)
-increases cardiac pumping ability
-decreases HR
2- diuretics (lasix)
-decrease vascular fluid volume
-decrease preload and after load
-control HTN


ACE inhibitors

Quinipril (accupril)
Captopril (capoten)
Enalopril (vasotec)
Lisinopril (zestril)
Fosinopril (monopril)
benazepril (lotensin)

Inhibit conversion of angiotensin I to angiotension II (inhibits vascular smooth muscle contraction)
-decreases Na retention and peripheral vasocontriction in order to decrease BP
-also prevents the inactivation of bradykinin (a vasodilator)
-result is arteriolar vasodilation, decreased peripheral resistance and increased flow

usually the 1st step in managing LV failure

can be used with diuretics and calcium channel blockers (for HTN, never for CHF or angina)

side effects:
-nonproductive dry cough
-decreased taste perception

adverse effects:
-excessive hypotension

May react with diuretics and cause hypotension.
-with potassium sparing diuretics, the problem may be hyperkalemia

step 2 with CHF is use of diuretics, especially loop diuretics (lasix)

step 3 with CHF is use of nonselective beta blocker and selective alpha 1 adrenergic blocker (carvedilol)

step 4: digoxin- when there is systolic dysfunction and arrhythmias




decreasepreload through peripheral vasodilation
-reduce myocardial oxygen demand
-reduce chest discomfort (angina)
-may also dilate coronary arteries, improve BF

side effects:
-flushing and headache
-reflex tachycardia

beta blockers and calcium channel blockers may also be used for angina


beta-adrenergic blocking agents

Non-selective beta-blockers:
-propanolol (inderl)
-nadolol (corgard)
penbutolol (levatol)


Selective beta blockers (beta-1)

*beta1 receptors in the heart
*beta2 receptors in the lungs and some arterioles

-reduce myocardial demand by reducing HR and contractility and SV
-control arrhythmias, chest pain
-reduce BP

should be avoided with certain kinds of angina, all COPD, and DM

patients should never suddenly discontinue use of BB since there a risk of sudden death from anginal attack

side effects:
-sleep disturbances
-mental status changes- depression, disorientation
-cold extremities

**patients taking BB- can't use HR to determine exercise tolerance **


Calcium channel blockers


inhibit flow of calcium ions
decrease HR
decrease contractility
dilate coronary arteries
reduce BP
control arrhythmias
chest pain

side effects:
-significant bradycardia
-peripheral vasodilation can cause flushing, headache, ankle swelling, and reflex tachycardia

drug interactions:
-verapamil can result in digoxin toxicity
-verapamil and BB together can cause cardiac depression and AV block



numerous drugs, 4 main classes

alter conductivity
restore normal heart rhythm
control arrhythmias
improve cardiac output

-quinidine (ACE)



cardiac glycosides

increases contractility and decreases HR
mainstay in the treatment of CHF (digoxin (lanoxin))

used as step 4 with CHF when there is a systolic dysfunctional and arrhythmias

increases the force of contraction of cardiac muscle without increasing oxygen demand
-EF may increase

adverse effects
-toxicity (signs: cardiac arrhythmia, anorexia, nausea, vomiting, mental status change (hallucinations, blurred vision))

PT** watch for digoxin toxicity



furosemide (lasix)
hydrochlorothizide (esidrix)

-decrease myocardial work (reduce preload and aferload)
-control HTN
-inhibit tubular reabsorption of sodium and chloride in the kidney, which in turn, inhibits water reabsorption and increases urine volume-->ultimate result is decreased vascular resistance

thiazides should NOT be used with the elderly or anyone with renal dysfunction

side effects:
-hyperglycemia especially with diabetes
-hyperuricemia- too much uric acid- gout
-increase in LDL

drug interactions:
-increases lithium reabsorption, which can increase lithium blood levels and result in lithium toxicity
-digoxin toxicity

Loop diuretics (furosemide (lasix), bumex, edecrin)
-inhibit sodium and chloride reabsorption in the lop of Henle
-more effective than thiazides
-may be used with elderly

potassium sparing diuretics:
-weak diuretics that prevent hypokalemia



decreases platelet aggregation

may prevent myocardial infarction

used in treatment of angina, CAD and to prevent MI

shouldn't be used after acute injury since it prolongs clotting


alpha adrenergic blockers

alpha 1 blockers: prazosin (minipress)
-blocks alpha1 receptors in smooth muscle allowing arterial and venous vasodilation

side effects:

alpha 2 blockers (clonidine (catapress))
-stimulate alpha 2 receptors in the brainstem, which decrease sympathetic NS signals with resulting decreased HR, peripheral resistance and BP

side effects:
-dry mouth



hydralazine (apresoline)

used in combo with ACE inhibitors ad have increased survival with CHF

can also be used with beta blockers to treat HTN

side effects:
-GI disturbances
-nasal congestion


activity restriction with acute MI

activity can be increased once the acute MI has stopped (peak in cardiac troponin levels)
limited to 5 METs or 70% of age predicted HRmax for 4-6 weeks following MI


activity restriction with acute heart failure

oxygen demand should not be increased in patients in acute or decompensated heart failure

gradual increase while monitoring hemodynamic response to activity


surgical interventions for heart disease

1- percutaneous transluminal coronary angioplasty (PTCA)

2- intravascular stents

3- coronary artery bypass graft (CABG)

4- transplantation

5- ventricular assist device


percutaneous transluminal coronary angioplasty


under fluoroscopy, surgical dilation of blood vessel using a small balloon tipped catheter inflated inside the lumen

relieves obstructed blood flow in acute angina or acute MI

results in improved coronary BF, improved LV function, anginal relief


intravascular stents

an endoprosthesis (pliable wire mesh) implanted postangioplasty to prevent restenosis and occlusion in coronary or peripheral arteries

often coated in medication to prevent thrombosis


coronary artery bypass graft


surgical circumvention of an obstruction in a coronary artery using an anastomosing graft (saphenous vein, internal mammary artery)

multiple grafts may be necessary

results in improved coronary BF, improved LV function, anginal relief


heart transplantation

used in end stage myocardial disease (cardiomyopathy, ischemic heart disease, valvular heart disease)

heteroptics: leaving the natural heart and piggybacking the donor heart

orthotopic: removing the disease heart and replacing it with donor heart


ventricular assist device

implanted device (accessory pump) that improves tissue perfusion and maintains cariogenic circulation

used with severely involved patients


occlusive peripheral arterial disease (PAD)

chronic, occlusive arterial disease of medium and large vessels, the result of peripheral atherosclerosis

associated with HRN and hyperlipidemia
-also CAD, CVA, DM, metabolic syndrome and a hx of smoking

diminished blood supply to affected extremities with decreased or absent pulses

color: pale on elevation, red in dependency

early stages: intermittent claudication
-pain: burning, searing, aching, tightness, cramping
-regularly and predictably with walking
-relieved with rest

late stages: pain with rest, muscle atrophy, trophic changes

critical stenosis PAD: patients exhibit resting or nocturnal pain, skin ulcers and gangrene


thromboangiitis obliterans (Buerger's disease)

chronic, inflammatory vascular occlusive disease of small arteries and veins

occurs commonly in young adults, largely males who smoke

begins distally and progresses proximally in both upper and lower extremities

patients exhibit paresthesias or pain, cyanotic cold extremity, diminished temperature sensation, fatigue, risk of ulceration and gangrene


raynaud's phenomenon

episodic spasm of small arteries and arterioles

abnormal vasoconstrictor reflex exacerbated by exposure to cold or emotional stress

fingertips exhibit pallor, cyanosis, numbness and tingling

largely affects females


varicose veins

distended, swollen superficial veins

tortuous in appearance

may lead to varicose ulcers


superficial vein thrombophlebitis

clot formation and acute inflammation in a superficial vein

localized pain; usually in saphenous vein


deep vein thrombophlebitis (DVT)

clot formation and acute inflammation in a deep vein

usually in LE - associated with venous stasis, hyperactivity of blood coagulation and vascular trauma; early ambulation is prophylactic, helps eliminate venous statis

-asymptomatic early
-progressive inflammation with tenderness to palpation
-dull ache, tightness or pain in calf
-skin discoloration and venous distention

may precipitate PE: presents abruptly with chest pain and dyspnea; diaphoresis, cough, apprehension

medical management: anticoagulation therapy (heparin)
-ambulation and mobility encouraged after 1 dose
-compression stockings


chronic venous stasis/incompetence

venous valvular insufficiency: from fibroelastic degeneration of valve tissue, venous dilation

I: mild aching, min edema, dilated superficial veins
II: increased edema, multiple dilated veins, changes in skin pigmentation
III: venous claudication, severe edema, cutaneous ulceration



enlargement of nodes, with or without tenderness



chronic disorder with excessive accumulation of fluid due to obstruction of lymphatics or removal of lymph nodes

causes swelling of the soft tissues

results from mechanical insufficiency of the lymphatic system

primary lymphedema: congenital condition with abnormal lymph node or lymph vessel formation (hypo/hyperplasia)

secondary lymphedema: acquired, due to injury of 1 or more parts of lymphatic system. Possible causes include:
-tumors, trauma or infection affecting lymph vessels
-radiation therapy with fibrosis of tissues
-chronic venous insufficiency
-in tropical and subtropical areas, filariasis (nematode worm larvae in lymphatic system)


exercise tolerance testing

determines the physiological responses during measured and graded exercise stress of increasing workloads
- determines exercise capacity of individual
- establishes basis for exercise prescription
- screens patients for possible CAD
- assists in the diagnosis of suspected cardiovascular disease

maximal ETT:
-defined by target endpoint HR

submax ETT:
-symptom-limited or terminated at 85% of age predicted HRmax
-used to evaluate early recovery of patients after MI, CABG or coronary angioplasty

continuous ETT:
-workload is steadily increased
-step test
-ramp test

discontinuous (interval) ETT:
-allows rest
-used for patients with more pronounced CAD

positive ETT:
-indicates O2 supply is inadequate to meet demand; positive for ischemia

negative ETT:
-balanced O2 supply and demand

false positive ETT:
false negative ETT:

Functional 6 minute walk test
-highly correlated to other ETT, sub max and max VO2


monitoring exercise and recovery; examine for:

appearance, S&S of excessive effort
-persistent SOB
-anginal pain
-severe leg claudication
-excessive fatigue
-pallor, cold sweat
-ataxia, incoordination
-pulmonary rales

change in HR- rise with workload, plateau just before VO2max

changes in BP
-SBP rise with workload
-DBP stay roughly the same

Rate pressure product

RPE: 6-20
-increases linearly
*important measure for pets who don't exhibit typical rise in HR with exercise (beta-blockers)

pulse oximetry

ECG normal changes
-rate-related shortening of QT interval
-ST segment depression, upsloping, 1mms indicative of myocardial ischemia


metabolic equivalents

MET= the amount of oxygen consumed at rest (sitting) = 3.5 mL/kg of body weight per minute

at rest, the body consumes about 200-250 mL of oxygen/minute = 1 MET

MET levels (multiples of resting VO2) can be directly determined during ETT; using collection and analysis of expired air

can be used to predict energy expenditure during certain activities

1.5-2 METs: standing, walking slowly (1mph)

2-3 METs: level walking (2mph); level bicycling (5mph)

3-4 METs: level walking (3mph); biking (6mph)

4-5 METs: walking (3.5 mph); biking 8mph

5-6 METs: walking briskly 4mph; biking 10 mph,

6-7 METs: walking very briskly 5mph; biking 11 mpg; leisurely swimming

7-8 METs: jogging 5 mph; biking 12 mph

8-9 METs running, biking 12 mph, swimming

>10 METs: running 6mph


guidelines for exercise prescription: TYPE

-cardiorespiratory endurance
-dynamic arm exercise (^HR and BP)
-aerobic activities: swimming

Early rehab: discontinuous/interval training with frequent rests progressing to continuous (allows patient to work at higher % of VO2 max)

Warm up and cool downs -- low intensity cardiorespiratory endurance, flexibility (5-10 minutes)

Resistive exercises:
-reserved for later cardiac rehab
-moderate intensities (60-80 of 1RM)
-monitor responses using RPP
-precautions: monitor BP, avoid valsalva's
-contraindicated for patients with uncontrolled HTN or arrhythmias

relaxation training


guidelines for exercise prescription: INTENSITY

% of functional capacity revealed on ETT
-within 40-85% range

-% of HRmax
-Karvonian's formula: more closely approximates the relationship between HR and VO2max- increased variability in patients on meds
-beta blocker and pacemaker: affects ability of HR to rise in response to exercise

RPE : 11-13 "light"



guidelines for exercise prescription: DURATION

conditioning phase may vary from 10-60 minutes depending on intensity

moderate intensity ~ 20-30 minutes


guidelines for exercise prescription: FREQUENCY

dependen upon intensity and duration

avg: 3-5 days/week for exercise at moderate intensities and duration (>5 METs)

daily or multiple daily sessions for low intensity (


guidelines for exercise prescription: PROGRESSION

modify if:
-HR is lower than target HR
-RPE is lower
-symptoms of ischemia (angina) don't appear

rate of progression depends on age, health status, functional capacity, personal goals, preferences

* as training progresses, duration is increased first, then intensity


consider a reduction in exercise with:

acute illness; fever, flu m

acute injury

progression of cardiac disease: edema, weight gain, unstable angina

overindulgence: food, caffeine, alcohol

environmental stressors: heat, cold, humidity,


absolute indications to terminate exercise

drop in SBP >10 mmHg

moderate to severe angina

increasing NS symptoms (ataxia, dizziness, near syncope)

signs of poor perfusion

technical difficulties in monitoring ECG or BP

subject's desire to stop

sustained VT

ST elevation >1 mm


relative indications to terminate exercise

ST or QRS changes (excessive ST depression) or marked axial shift

arrhythmias other than sustained VT

fatigue, SOB, wheezing, leg cramps or claudication

development of bundle branch block that can't be distinguished from VT

increasing chest pain

hypertensive response (SBP >250 or DBP >115)


exercise prescription post percutaneous transluminal coronary angioplasty:

wait to exercise vigorously ~2 weeks post PTCA to allow inflammatory process to subside

walking program can be initiated immediately

use post PTCA ETT to prescribe exercise


exercise prescription post CABG

limit UE exercise while sternal incision is healing

avoid lifting, pushing, pulling for 4-6 weeks post


absolute contraindications for cardiac rehab

acute MI (within 2 days)

unstable angina not previously stabilized by medical therapy

uncontrolled cardiac arrhythmias causing symptoms or hemodynamic compromise

acute PR or pulmonary infarction

acute myocarditis or pericarditis

acute aortic dissection


relative contraindications for cardiac rehab

L man coronary stenosis

moderate stenotic valvular heart disease

electrolyte abnormalities

severe arterial HTN

tachyarrhythmias or bradyarrhythmias

hypertrophic cardiomyopathy and other forms of outflow tract obstruction

mental or physical impairment leading to inability to exercise adequately

high degree AV block


phase I: inpatient cardiac rehab (Acute)

length of stay ~ 3-5 days for uncomplicated MI (no persistent angina, malignant arrhythmias or heart failure)

-initiate early return to independence in ADLs (typically after 24 hours or until patient is stable for 24 hours)
-counteract deleterious effects of bed rest; reduce risk of thrombi, maintain muscle tone, reduce orthostatic hypotension, maintain joint mobility
-help allay anxiety
-provide education
-promote risk factor modification

Exercise guidelines:
-ADLs, selected arm and leg exercises, early supervised ambulation
-initial activities: low intensity (2-3 METs) progressing to >5 METs by discharge
-post MI: limited to 70% HR max and/or % METs until 6 weeks post-MI
-short exercise sessions, 2-3x/day
-Post-surgical patients: progressed more rapidly than post-MI, unless peri-operative MI ; lifting activities are restricted for 6 weeks

-understanding of cardiac disease, risk factor modification
-self monitoring procedures, warning signs or exertion intolerance
-energy costs, fatigue, guidelines, pacing, HEP

-low risk patients: gradual increase in ambulation: goal of 20-30 minutes, 1-2x/day, 4-6 weeks post MI


Phase II: outpatient cardiac rehab (subacute)

Eligible patients:
-MI/acute coronary syndrome
-Stable angina
-heart valve surgical repair/replacement
-heart or lung replacement
-heart failure and PAD

-improve functional capacity
-progress toward full resumption of ADLs and occupational activities
-promote risk factor modifications
-encourage pacing, energy conservation

-frequency: 2-3x/week
-duration: 30-60 min with 5-10 warm up/cool
-patients gradually weaned from continuous monitoring to spot checks and self monitoring
-suggested end point: 9 MET functional capacity (5MET capacity is needed for safe resumption of most daily activities)

strength training: after 3 weeks cardiac rehab, 5 weeks post-MI or 8 weeks post CABG
-begin with elastic bands and light hand weights (1-3 lbs)


phase III: community exercise programs (post acute, post discharge)

-improve/maintain functional capacity
-promote self regulation of exercise program
promote life long commitment to risk factor modification

Exercise guidelines:
-entry level: 5 METs, stable angina, medically controlled arrhythmias during exercise
-progression: supervised to self-regulation
-progress to 50-85% of functional capacity, 3-4x/week, 45 min or more
-discharge 6-12 months


resistance exercise training

-permitted if remain under 70% HRmax or 5 METs for 6 weeks post MI
-cautious of valsalva

Cardiac surgery:
-LE can be initiated right away in absence of peri-operative MI
-UE resistance training avoided until soft tissue and bony healing has occurred: 6-8 weeks

Post transcatheter procedure (PTCA, etc)
-min of 3 weeks following procedure and 2 weeks of consistent participation in a supervised CR endurance training program


exercise prescription for patients with heart failure

patients demo significant ventricular dysfunction, decreased CO and low functional capacities

assess for signs of decompensation at each visit: increased SOB


exercise prescription with cardiac transplant

patients may present with:
-exercise intolerance due to extended inactivity
-side effects from immunosuppressive drug therapy: hyperlipidemia, HTN, obesity, diabetes, leg cramps
-decreased LE strength
-increased fracture risk due to long term corticosteroid use

HR is no an appropriate measure of intensity

longer periods of warm up and cool down


exercise prescriptions with pacemakers and automatic implantable cardioverter defibrillators (AICDs)

pacemakers are programmed to pace HR

AICDs will deliver electric shock if HR exceeds set limit and/or ventricular arrhythmia is detected

avoid UE aerobic or strengthening exercises for 4-6 weeks after implant to allow the leads to scar down


exercise training for patients with PAD

may result in improved functional capacity, improved peripheral BF via collateral circulation and muscle oxidative capacity

consider interval training with frequent rests

walking program:
-intensity such that patients reports 1 on claudication scale within 3-5 minutes; stopping if they reach 2 (until pain subsides)
-total of 30-60 minutes (intervals)
-3-5 days/week
-record time and onset of pain and duration

beta blockers for treatment of HTN may decrease time to claudication or worsen symptoms

aspirin and warfarin may improve time to claudication

high risk for CAD


rehab guidelines for patients with chronic venous insufficiency

1- Edema management:
positioning: (min of 18 cm above heart); avoid dependent position

compression therapy
-bandages applied within 20 minutes of rising
- paste bandage (Unna boot): 4-7 days
-graduated compression stockings (at least 30 mmHg)
-compression pump- 1-2 hours/day

red flag: consider consequences of compression to a limb with an ABO


phase I management of edema secondary to lymphatic dysfunction:

short stretch compression bandage- 24 hours/day

manual lymph drainage with complete decongestive therapy
-massage and PROM to assist lymphatic flow
-decongest proximal segments first, then extremities, directing flow distal to proximal
-compression using multilayered padding and short stretch bandages

functional activities
-walking, cycling
-water based
-tai chi and balance
-ADL training
-RED FLAG: strenuous activities, jogging and ballistic movements are contraindicated-- likely to exacerbate lymphedema

signs of lymph overload: discomfort, aching or pain in proximal lymph areas, change in skin color

meticulous skin care

contraindicated modalities:
-ice, heat, hydrotherapy, saunas, contrast baths, paraffin-- all cause vasodilation and increase lymphatic load of water

compression garments at end of phase I
-RED FLAG: excessively high pressures will occlude superficial lymph capillaries and restrict fluid absorption


Phase II management (self-management) of lymphedema

skin care
compression garments
lymphedema bandaging at night
MLD as needed
compression pumps; with caution

RED FLAG: pressures >45 mmHg are contraindicated- can cause lymphatic collapse; contraindicated with soft tissue injury

-skin and nail care
-self bandaging
-infection management
-maintain exercise


shock (hypoperfusion)

failure of the circulatory system to perfuse vital organs

at first blood is shunted from the periphery to compensate
-may lose consciousness
-HR increases, increased O2 demand

Types of shock:
-hemorrhagic: severe internal or external bleeding
-psychogenic: emotional stress causes blood to pool in body away from the brain
-metabolic: loss of body fluids from heat or severe vomiting or diarrhea
-anaphylactic: allergic reaction from drugs, food or insects
-cardiogenic: MI or cardiac arrest results in pump failure
-respiratory: respiratory illness or arrest results in insufficient oxygenation of the blood
-septic: severe infections cause blood vessels to dilate
-neurogenic: TBI, SCI or other neural trauma causes disruption of ANS resulting in disruption of blood vessel dilation/constriction

-pale, gray or blue, cool skin
-increased, weak pulse
-increased RR
-decreased BP
-irritability or restless
-diminishing level of consciousness


anti-cholinergic drugs

used with IV for heart block or bradycardia

inhibit acetylcholine at the parasympathetic nerves, blocking vagal effects on SA and AV nodes of the heart

Side effects:
-dry mouth
-blurred vision

Ex: atropine


heart block

when the spread of electrical excitation to the heart is interrupted or slowed

atropine (anti-cholinergic med) is given


heart failure

when the heart muscle is unable tot adequately pump blood to maintain proper circulation

-R heart affected-- peripheral edema
-L heart affected-- pulmonary edema
-if severe-- edema may be widespread



area of necrotic tissue that results from a loss of blood supply to that area



the obstruction of circulation that results in a temporary deficiency of blood supplied to a certain area of the heart muscle

usually causes pain in chest (angina)



proteins that carry fat in the blood for delivery to the cells

low density lipoproteins (LDL)-- associated with arterial damage

high density lipoproteins (HDL)-- promote the removal of cholesterol by the liver
-engaging in moderate aerobic exercise may elevate HDL levels

LDL/HDL ratio is important in reducing risk of heart disease


serum enzymes

appear in the circulation following death of cardiac muscle cells

creatine phosphate (CPK)

lactate dehydrogenase (LDH)

serum glutamic oxalacetic transminase (SGOT


criteria to terminate inpatient exercise

fatigue, lightheadedness, confusion, ataxia, pallor, cyanosis, dyspnea, nausea, onset of angina with exercise

ST displacement (2mm) horizontal or downsloping from rest level

ventricular tachycardia or >3 consecutive PVCs

drop of SBP of >20mmHg during exercise

rise in SBP >220 mmHg or DBP >110 mmHg


lymphatic system

includes: lymphatic vessels, lymph fluid, lymph tissues, and organs (nodes, tonsils, spleen, thymus and thoracic duct)

lymph contains excess interstitial fluid, WBC, and some proteins

almost all tissues have lymphatic vessels except superficial portions of the skin, the CNS and bones

lymphatic vessels accompany arteries and veins, and drain lymph from bodily tissues and return it to the venous circulation

the R lymphatic duct drains the R arm, R side of the head and R side of the thorax into the R subclavian vein

The rest of the body drains into the thoracic duct, which empties into the L subclavian vein

major lymph nodes: submaxillary, cervical, axillary, mesenteric, iliac, inguinal, popliteal and cubital