Cardiovascular diseases and cardiac rehab Flashcards
artherosclerosis
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
2-MI
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
- myopathies
- osteoporosis
pathophysiology:
- decreased CO
- elevated end diastolic pressures (preload)
- tachycardia
- 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
- orthopnea
- paroxysmal nocturnal dyspnea
- pulmonary rales, wheezing
S&S of low CO:
- hypotension
- tachycardia
- lightheaded/dizzy
- 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
S&S:
- dependent edema
- weight gain
- ascites (abnormal abdominal fluid retention)
- liver engorgement (hepatomegaly)
- anorexia, nausea, bloating
- cyanosis
- 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
diuretics
sodium restriction
measures to improve myocardial contractility and correction of arrhythmias
meds: 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
- hyperkalemia
- angioedema
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
nitrates
nitroglycerin
decreasepreload through peripheral vasodilation
- reduce myocardial oxygen demand
- reduce chest discomfort (angina)
- may also dilate coronary arteries, improve BF
side effects:
- dizziness
- 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)
**-olol
Selective beta blockers (beta-1)
- lopressor
- atenolol
- beta1 receptors in the heart
- beta2 receptors in the lungs and some arterioles
“anti-hypertensives”
- 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
procardia
norvasc
cardizem
verapamil
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
anti-arrhythmics
numerous drugs, 4 main classes
alter conductivity
restore normal heart rhythm
control arrhythmias
improve cardiac output
ex:
- quinidine (ACE)
- procanamide
digitalis
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
diuretics
THIAZIDES
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
- hypokalemia
- hyperuricemia- too much uric acid- gout
- increase in LDL
- hypercalcemia
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
aspirin
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:
- syncope
- headache
- palpitations
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
- sedation
- depression
vasodilators
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
- headache
- flushing
- 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
PTCA
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
CABG
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
S&S
- asymptomatic early
- progressive inflammation with tenderness to palpation
- dull ache, tightness or pain in calf
- swelling
- warmth
- skin discoloration and venous distention
may precipitate PE: presents abruptly with chest pain and dyspnea; diaphoresis, cough, apprehension
*emergency
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
classification:
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
lymphadenopathy
enlargement of nodes, with or without tenderness
lymphedema
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:
- surgery
- 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
- safer
- 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
- dizziness/confusion
- 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
- tachycardia
- 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
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
HR
- % 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”
METs
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)
GOALS:
- 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
Education:
- understanding of cardiac disease, risk factor modification
- self monitoring procedures, warning signs or exertion intolerance
- energy costs, fatigue, guidelines, pacing, HEP
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
- CABG
- PCI
- Stable angina
- heart valve surgical repair/replacement
- heart or lung replacement
- heart failure and PAD
GOALS:
- improve functional capacity
- progress toward full resumption of ADLs and occupational activities
- promote risk factor modifications
- encourage pacing, energy conservation
GUIDELINES:
- 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)
Goals:
-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
post-MI:
- 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 exercise 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
education:
- 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
S&S:
- pale, gray or blue, cool skin
- increased, weak pulse
- increased RR
- decreased BP
- irritability or restless
- diminishing level of consciousness
- nausea/vomitting
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:
- palpitations
- headache
- restlessness
- ataxia
- 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
CHF
- R heart affected– peripheral edema
- L heart affected– pulmonary edema
- if severe– edema may be widespread
infarction
area of necrotic tissue that results from a loss of blood supply to that area
ischemia
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)
lipoproteins
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
