what must a doctor do before putting a patient on quinadine
they need to digitilize the person first because the dig takes care of the heart rate.
extends refractory period
Norpace side effects
Lidocaine for the heart
has to be preservative free (No epinephrine)
makes it harder for a patient to go into a v fib
prevents patient from going into v tach
anestasizes the heart
0.5-1 mg/kg depending on your person
lidocaine IV can cause
push over 1-2 minutes (preferably 2 minutes)
can cause confusion (especially in elderly)
can get a psychosis
possible blocks and arrests
important about lidocaine
make sure you pick the right lidocaine
make sure you put it in its own line. Do not mix with other drugs in IV line
class 1 C drugs.
This class of drugs are used when other things don't work.
Used for PAF, Life threatening ventricular arrhythmias. 150 to 300 mg po q. 8hrs.
Monitor for increase in arrhythmias, CNS effects ( dizziness, anxiety, ataxia, confusion, and seizures.
Used for life threatening ventricular arrhythmias. Can cause new or worse arrhythmias. CHF because of negative inotropic effect. Use for AF, PSVT.
100mg po BID. Maximum dose of 400 mg.
Monitor for increase & severity of arrhythmia. Monitor for CHF, tremors,
dizziness and visual disturbances.
class 1 c drugs
. Flecainide (Tambacor)
. Propafenone hydrochloride ( Rythmol )
. Most potent Class I agents. Slows conduction through atria , purkingee
system and ventricals. Decreases repolarization rate. Decreases contractility.
. Causes decrease in PVCS and VT
class 2 Beta blockers
. Only group of antiarrhythmics shown to prolong life
. Beta 1 receptors in heart attach to calcium channels. Blockage decreases Ca++
influx. Depresses phase 4 of depolarization. Decreases automaticity, heart rate,
and BP. Decreases AV conduction.
. Propranolol ( Inderal )—non selective
. Metoprolol ( Lopressor )---selective
. Atenolol ( Tenormin )
. Sotalol ( Betapace )
. CV: Bradycardia, hypotension, edema, CHF, Pulmonary Edema ,
. Resp: Bronchospasm
. CNS: Fatigue, weakness, dizziness, mental changes, insomnia, confusion
. GI: Constipation, diarrhea, nausea, vomiting
. GU: Impotence
endocrine: blood sugar variations
negative inotropic effect causes
dromotropic effect causes
(1) Refers to a change in the speed of conduction through the AV junction
(2) A positive dromotropic effect results in an increase in AV conduction velocity
(3) A negative dromotropic effect results in a decrease in AV conduction velocity
(1) Refers to a change in myocardial contractility
(2) A positive inotropic effect results in an increase in myocardial contractility
(3) A negative inotropic effect results in a decrease in myocardial contratility
(1) Refers to a change in heart rate
(2) A positive chronotropic effect refers to an increase in heart rate
(3) A negative chronotropic effect refers to a decrease in heart rate
interactions with Beta Blockers
. Caution with other antiarrhythmics. Can cause additive effects.
. NSAIDS may decrease antihypertensive effect.
. Cimetidine can increase the effect of inderal.
. In diabetics can mask signs of hypoglycemia.
nursing considerations for Beta Blockers
. Monitor vital signs frequently during period of adjustment. Notify MD if pulse
falls below 50 to 60 beats / minute and / or SBP falls below 90 to 100.
. If meds given IV must be on a monitor during administration and for several
hours later. Monitor hepatic, renal and CBC function.
. Monitor I&O, daily weight, and check for CHF.
. Give with meals or immediately after eatting. Extended release tablets should
be swallowed whole. Do not crush.
potassium channel blockers
Action: Block potassium channels, prolong repolarization and refractory
periods. They effect fast tissue and commonly are used to manage
difficult to treat arrhythmias.
Agent: Amiodarone ( Cordarone)
Ibutilide fumarate ( Corvert )
potassium channel blockers
. Treatment of life threatening recurrent V-Fib and hemdynamically unstable
V-Tach and SPVT, AF, PAF.
Dose: PO—800 to1600 mg/ day for 1 to 3 wk and reduce to 600 to 800 mg/ day
for 5 wks: usual maintenance dose, 400 mg/ day.
IV: Give through central line if possible.
contraindications of potassium channel blockers
. Severe sinus bradycardia since drug slows heart rate by interfering with SA
nodal firing. AV nodal blockage since drug slows conduction through AV
node. May cause complete heart block resistant to atropine.
precautions for potassium channel blockers
CHF may be worsened. Hypokalemia may block amiodarone action.
Side Effects / Adverse reactions:
. CNS—ataxia, tremors
. CV-----SA & AV blockage, bradycardia, myocardial depression, IV-hypotension
. EYE---small corneal deposits that can impair vision may develop with long term
use. When drug is discontinued deposits may slowly disappear.
. GI------anorexia, nausea, constipation, abdominal pain
. PULMONARY—pulmonary fibrosis, pneumonitis
. SKIN---light sensitivity caused by crystals deposited in the skin producing a
nursing considerations for potassium channel blockers
. Assess EKG , BP and pulse
. Assess lung sounds. Rales, decreased lung sounds or friction rub may indicate
pulmonary toxicity. Check weight, I&O and signs of CHF
. Check skin for bluish coloration. Check gait and check for tremors
. Eye exam should be done before and at regular intervals during therapy. Avoid
sunbathing, tanning salons because of photosensitivity. Limit outdoor activity
between 10 am and 2 pm.
. Increase dietary intake of fruit, fiber , fluids and exercise to combat
. Missed dose: Omit. Do not double up on missed dose. Notify MD if two or
more doses are missed.
potassium channel blocker
Used for AF, Atrial Flutter. 1mg IV over 10 min. for patients > 60kg. 0.01mg/kg for patients < 60 kg over 10 mg min. Stop infusion as soon as arrhythmia is stopped or if sustained VT or marked QT prolongation.
class 1 sodium channel blockers
. Decrease rate of conduction
. Prolongs action potential duration
. Reduces speed of impulse conduction
. For atrial and ventricular dysrhythmias
. Procainamide ( Pronestyl )
. Disopyramide ( Norpace )
. Quinidine ( Quinidex )
indications of sodium channel blockers
ex: PROCAINAMIDE (PRONESTYL )
. Stable ventricular tachycardia
. Premature ventricular contractions
. Ventricular fibrillation
. PSVT, PAT, Junctional tachs. ,
. Atrial flutter and fibrillation
actions of sodium channel blockers
. Slows conduction. Is a negative inotrope with a ischemic myocardium
. Decreases myocardial excitability
. Is often used as drug of choice if resistance to lidocaine
Contraindicated in patient with myasthenia gravis.
Caution with patients with MI, CHF, Digoxin intoxication.
adverse effects of sodium channel blockers
. Myocardial depression. Prolongs duration of QRS, QT interval, AV
. Hypersensitivity. Confusion, seizures, dizziness.
. Hypotension if given too fast IV. Blood dyscrasias like thrombocytopenia.
. Gastric: anorexia, diarrhea, nausea, vomiting.
. PO: Give with meals or snack to lessen GI distress.
. Monitor EKG, BP, and pulse continously throughout IV administration.
. Keep patient supine during IV admininstration. Assess QRS and QT intervals.
. When IV, discontinue if QT increases by 50% or PR more than .20 second or if
BP drops 15mm Hg.
. Slows conduction through cardiac tissue. Refractory period is lengthened
especially in atria. Used for atrial flutter or fibrillation to maintain sinus
. Has anticholinergic effect by inhibiting vagal action on SA and AV nodes.
Sinus node may accelerate causing a dangerous sinus tachycardia. If
Quinidine is given to people with A. Flutter or A. Fibrillation, they should be
digitalized first to slow the SA and AV nodes.
. Quinidine Sulfate—200 to 400 mg every 4 to 6 hours.
. Sustained release ( Quindex Extentabs—300 to 600 mg every 8 to 12 hours.
. Quinidine Gluconate—324mg every 6 to 8 hours.
. Quinaglute 324mg every 6 to 8 hours IM or IV
. Most common effect is diarrhea. May have nausea and vomiting.
. Can cause thrombocytopenia.
. Hypotension, tinnitus, vertigo, visual disturbances, confusion, psychosis.
. Arrhythmias like SA and AV blocks, sinus arrest.
. Asthma like symptoms. Systemic Lupus like symptoms.
. Will increase digoxin levels. Nifedipine will decrease Quinidine levels.
. Prior to giving drug need baseline QT interval since drug can prolong it.
. Give with meals to decrease GI upset. Do not crush sustained release.
. Monitor vital signs, EKG and intake and output. Monitor platelets.
. Monitor for CHF.
DISOPYRAMIDE ( NORPACE )
. Prolongs refractory period. Decreases myocardial contractility. Has
anticholinergic effect so patients with A. Flutter and A. Fibrillation
should be digitalized first.
. Neuro: Blurred vision, dizziness, headache, agitation, depression.
. Cardio: Conduction disturbances, hypotension, chest pain, CHF, fatigue,
edema, weight gain.
. GI: Dry mouth, constipation, nausea, pain, bloating, anorexia, diarrhea.
. Resp: SOB
. Renal: Urinary retention, hesitancy,and frequency
. Endocrine: Hypoglycemia
. Monitor vital signs, EKG, QRS and QT intervals, I and O, weight.
. Monitor for CHF. Check platelets.
. Sugarless gum for dry mouth
. Take on empty stomach
. Eat high fiber diet. Bulk laxatives to treat constipation.
. Monitor potassium levels. Ineffectve in hypokalemia. Toxic with hyperkalemia.
class 1 b drugs
. Lidocaine (Xylocaine)
. Tocainide ( Tonocard)
. Mexiletine ( Mexitil)
LIDOCAINE ( XYLOCAINE )
. Elevates ventricular fibrillation threshold
. Treats symptomatic PVCS. Suppresses ventricular tachycardia.
. Adult: 1mg/kg to 1.5 mg/kg bolus IV followed by 0.5 mg to 0.75/kg in 10 minutes. About 50 to 100mg. Reduce bolus dose by 5% in patients with CHF.
. Infusion rate is 1 to 4 mg/minute. Can give endotracheal if IV not available.
. Onset of action is 30 to 60 seconds IV
. Therapeutic level is 1.5 to 6 ug/ml
. CNS: Paresthesias, numbness, agitation, confusion, seizures.
. CV: Hypotension, bradycardia, cardiac arrest, arrhythmias
. GI: vomiting
. Integ: Phlebitis
. Monitor vital signs, EKG, QRS and QT levels
. Monitor serum levels. Signs of toxicity include confusion, excitation, blurred
or double vision, nausea, vomiting, tinnitus, tremors, convulsions, difficulty
. Use only 1% or 2% solutions without epinephrine or preservative.
. Administer over 1 to 2 minutes . If given too fast, increase risk of seizures.
. Use infusion pump. Do not mix with other drugs.
calcium channel blockers (class IV)
Action: These drugs work by inhibiting the slow channel pathways or the calcium
Dependent channels. By doing this they depress phase 4 depolarization.
Therefore these drugs:
. Prolong AV node effective refractory period
. decrease AV node conduction and reduce rapid ventricular conduction
due to A. Flutter, AF. Used for SVT
. Ditiazem ( Cardizem )
. Verapamil ( Calan )
DILTIAZEM ( CARDIZEM )
. Temporary control of rapid ventricular response in a patient with A. FIB or
A. Flutter. Supraventricular arrhythmias
. Vasospastic angina. Essential Hypertension
. Unlabled use—prevention of reinfarction in non Q wave MI
. Hypersensitivity, sick sinus syndrome, 2nd or 3rd Heart , severe hypotension ( less
than 90/60 ). Patients undergoing cranial surgery, bleeding aneurysms
. CHF especially if on beta blocker. Conduction abnormalities. Renal or
. IV—bolus dose 0.25mg/kg over 2 minutes; second dose 0.35mg/kg over
2 minutes after 15 minutes prn; then 5-10 mg/hr or higher by continuous
. PO---usual dose 180 to 360 mg/day in divided doses or 60 to 120 mg
Adverse / Side effects:
. CNS—headache, fatique, dizziness, drowsiness, nervousness, insomnia,
confusion, tremor, gait abnormality
. CV—edema, arrhythmias, angina, 2nd and 3rd degree heart block, bradycardia,
CHF, hypotension, palpitations, syncope, flushing
. GI –nausea, constipation, anorexia, vomiting, diarrhea, impaired taste,
. Increases digoxin levels. Additive effects on AV conduction with beta blocker.
. Cimetidine can increase cardizem levels
. Withhold drug if SBP is< 90 or diastolic is < 60 . Monitor for arrhythmias, heart
blocks. Position changes slowly. Avoid driving until reaction to drug is known.
Keep follow up appointments.
. PO—AC and HS. IV—may be given direct as bolus over 2 minutes. May be
continuous IV infusion. Recommended rate-5 to 15 mg/hr. Can add to D5W,
NS and combos.
VERAPAMIL ( CALAN )
Dose: . PO—start with 80mg 3 to 4 times daily; daily range 240 to 480 mg..
. IV---5 to 10 mg bolus over 2 minutes; repeat dose of < 10 mg may be given after
. Beta blockers increase risk of CHF, bradycardia,heart block
. Increases digoxin levels.
. Lithium and cyclospore may be increased to toxic levels.
. PO—with food to decrease GI ditress. Capsules can be opened & sprinkled on
food. Do not dissolve or chew capsule.
. Transient asymptomatic hypotension may accompany IV bolus. Have patient
remain in recumberant position for at least 1 hour after dose.
. Same as with cardizem
ADENOSINE ( ADENOCARD )
. Slows impulse formation in SA node. Slows conduction time through AV node.
Depresses left ventricular function and restores NSR.
. General cardiac depressant
. Paroxysmal supraventricular tachycardia
. Sick sinus syndrome may be worsened by drug and produce sinus arrest
. IV—6 mg by rapid push with saline flush over 1 to 2 seconds. If not effective,
12 mg by rapid push may be given 2 minutes later; repeat once if necessary
. Arrhythmias , flushing, heart block, chest pain, SOB, cough, dizziness ,
numbness, tingling in arms.
. Continuous EKG. Monitor BP and pulse, lung sounds, respiratory
Used for bradycardia and heart block. 0.5 to 1mg IV bolus may be repeated every 3 to 5 min up to 0.04mg/kg. Monitor heart rate and rhythm. Assess for chest pain, urinary retention.
force of contraction
positive inotropic increases the force
negative inotropic decreases the force
negative dromotropic slows conduction
positive dromotropic speeds up contraction
conduction goes from arrythmia to heart block
heart rate (can go both ways)
positive chronotropic speeds up heart rate
negative chronotropic slows down heart rate
if contraction not forceful enough blood backs up causing heart failure
when starting a drip
know baseline QT interval
if there is 50% or more distance between 2 complexes
may be a block
used for every rhythm that has a T wave
only for v fib (only only only)
before you shock someone yell all clear and make sure you are not touching the patient
sodium channel blockers
decreases etopic beats from starting
5mg (3 bolus') then PO
if adenosine doesnt work
anatomy and physiology of an MI
. Sudden blockage of one of the branches of
the coronary arteries. When blood flow
acutely decreases by 80% to 90% ischemia
b. If blood flow is not restored myocardial
tissue necrosis can happen over a period
what rhythm are patients usually in with an M.I.
M.I. anatomy and physiology
Can result in sudden death or gradual
scarring over necrotic area.
d. Most MIs are secondary to thrombus
formation. Other factors are coronary
artery spasm, platelet aggregation, and
e. Cardiac cells can withstand ischemia
about 20 minutes before injury occurs.
during an M.I.
Within 4 to 6 hours the entire thickness of
the heart will become necrotic.
Around the area of infarction there are
Zone of Injury
Zone of ischemia
necrotic tissue is
zone of ischemia
really electrically unstable
thats why the first 72 hours after an M.I. is so important because that ischemic tissue is so unstable and arrthymic
acute coronary syndrome
•When ischemia prolonged and not immediately reversible, ACS develops.
•Encompasses a spectrum of unstable angina, non-ST segment elevation Myocardial Infarction ( NSTEMI ) and ST segment elevation Myocardial In farction.
•Reflects the relationship among these disorders.
pathology of an MI
•Ischemia causes a decrease in cardiac functioning.
•Can produce a permanent loss of contractile function in the injured area.
•Cardiogenic shock can develop from decreased cardiac output and decreased contractility and pumping capacity.
•Actual extent of MI depends on collateral circulation, anaerobic metabolism and workload demands on the myocardium.
give Over 5 minutes
if too fast causes seizures, blocks, hypotension
anterior wall MI
absolute worst MI
. Obstruction of left anterior descending
artery. 25% of all MIs. Highest mortality.
b. Most likely to cause left ventricular heart
failure and ventricular dysrhythmias.
c. People with anterior MI more likely to die
in the first year after the MI than those with other
d. EKG shows ST elevations, abnormal Q waves.
inferior wall MI
Results from occlusion of right coronary
artery. Is 17% of all MIs. 10% mortality
b. About 1/3 have right ventricular MI and
right ventricular failure.
c. EKG can show ST and T wave changes and
(T wave inverts, thats NOT NORmal)
posterior and lateral wall MI's
•Result from obstruction of the circumflex
•Posterior MI is 2% all MIs. Is uncommon.
•Lateral wall MIs have the least complications.
gender differences in acute coronary syndrome
Men are developing CAD at a younger age
than women and their death rates are
b. Initial cardiac event is more often MI than
c. Have higher rate of left ventricular
d. Have greater collateral circulation.
gender differences in acute coronary syndrome
CAD causes more deaths in women than
men. Usually older and sicker with first
b. Initial cardiac event more often angina.
c. After menopause risk of MI quadruples.
Prior to menopause have higher HDL levels
than men. After, LDL levels increase.
Fewer women than men present with
classic symptoms of MI. Fatigue often
1st sign of ACS. C/o palpitations more
e. More likely to experience fatal cardiac
event within 1st year after an MI.
f. Delay longer before seeking medical help.
•Have higher mortality rate and
complications after CABG surgery.
h. Those on oral contraceptives and who
smoke at greater risk for MI.
gerontologic considerations with an MI
•May have decreased responses to neurotransmitters so often pain is atypical. May have jaw pain of faint.
•Have had time to develop collateral circulation so may not have lethal complications.
cultural and ethnic consideration for MI's
•White, middle-aged men have highest incidence of CAD.
•African Americans have early age onset od CAD.
•African American women have higher incidence and death rate r/t CAD than white women.
•African Americans have more severe CAD than whites.
•Native Americans under 35 yrs have twice heart disease mortality as other Americans r/t obesity and diabetes.
•Hispanics have lower death rates from heart disease than non Hispanic whites.
Risk Factors for CAD
Gender (men > women until 60 yr)
Ethnicity (whites > African Americans)
Genetic predisposition and family history of heart disease)
•Modifiable Risk Factors:
Elevated serum lipids
Hypertension: 140/90 or greater
Obesity: waist circumference greater than 39.8 in men & 34.3 in women.
Fasting blood sugar > 110 mg/di
Homocysteine levels-if elevated can contribute to atherosclerosis
stages of MI healing
•Onset until 3rd day
Acute tissue degeneration. Infarct area
soft, mushy & necrotic. Dead tissue
electrically inert. Peri-infarct area ischemic
and electrically unstable.
Critical time period-majority of deaths
stages of MI healing
•4th to 7th day:
Softening of infarct area. Danger of
•8th to 10th day:
Newly formed capillaries develop around
infarct but it is 2 to 3 weeks before any
stages of MI healing
•11th day on:
Collagen forms about 12th day. Rupture
of ventricle possible from onset 14th day.
Takes 3 to 4 weeks before scar is firm.
Takes 2 to 3 months before scar is at
clinical manifestations of an MI
•Severe continuous chest pain not relieved by nitroglycerine or rest.
•Shortness of breath, pallor, cold clammy diaphoresis, dizziness, nausea, vomiting, BP changes, dysrhythmias, cyanosis, restlessness, and intense anxiety.
•Women may experience heaviness, squeezing type of chest pain. May have sharp, fleeting pain that returns. May have pain in jaw, neck, back & shoulder. Often have palpitations, may faint, nausea & vomiting
Deviations in the manifestations of an MI
•Patients with diabetes may have dull pain r/t neuropathies.
•African Americans may have dyspnea as major symptom.
•Elderly may have mild or absent pain. May have associative symptoms like SOB. Patients over 80 may display confusion or disorientation with decreased cardiac output.
•Electrocardiogram-serial readings to monitor evolution of MI.
•Troponin Levels-establishes diagnosis of MI.
•Cardiac Enzymes-CK (Creatine Kinase).
•White blood cell count, sedimentation rate
•Coronary Angiography- patient with NSTEMI may have this to evaluate extent of MI.
•Stress Test & Echocardiograms-may need to do dobutamine (Dobutex) stress echocardiogram if patient unable to exercise.
with an MI the
st segment elevates
T wave inversion
with ischemia of the heart
st segment depression
T wave inversion
what meds do they hold for Heart tests
usually beta blockers
goals for med management of MI
•Minimize myocardial damage, relieve pain & provide rest
emergency management of an MI
•Ensure patent airway. Oxygen at 2 to 4 L via nasal cannula.
•Insert 2 IV catheters.
•Obtain ECG. Place on monitor.
•Assess for pain (PQRST)
•Nitro. sl and aspirin if not already done by EMTs. Morphine for pain.
•Baseline blood work (cardiac markers) & chest xray
•Assess for antiplatelet, anticoagulant, and thrombolytic therapy.
•Give beta blocker and antidysrhythmic drugs as needed.
ongoing monitoring of an MI
•Monitor vital signs, level of consciousness, cardiac rhythm, and O2 sat
•Monitor response to medications. Remedicate or titrate medications as indicated.
•Provide emotional support and reassurance to patient and family.
•Explain all procedures/interventions to patient in simple terms.
•Anticipate need for intubation if respiratory distress is evident.
•Prepare for CPR, defibrillation, cardioversion and transcutaneous pacing as indicated.
•Used to dissolve the thrombi in coronary arteries and to restore blood flow.
•Most effective if done within 4 to 6 hours after start of chest pain where there is evidence of hyperacute or acute ECG changes in 2 or more leads.
•Works directly or indirectly to convert plasminogen to plasmin, an enzyme that acts to digest the fibrin matrix of clots.
Thrombolytic side effects/adverse reactions
•Hemorrhage and anemia
•Periorbital swelling, itching, urticaria, headache
contraindications for thrombolytic therapy
Active internal bleeding
History of cerebral aneurysm, brain tumor,
previous cerebral hemorrhage
Ischemic stroke within 3 months.
Significant closed head or facial trauma
within 3 months
Active peptic ulcer disease
Current use of anticoagulants
Ischemic stroke over 3 months ago,
dementia, intracranial pathology
Recent internal bleeding within 2 to 4
weeks. Serious systemic disease.
Uncontrolled hypertension over 180/110
Patients who weigh less than 65 kg have to
dose adjusted because of increased
likelihood of bleeding.
nursing implications of thrombolytic therapy
•Prior to treatment:
Assess vs, neuro, and cardiac rhythm.
Patient needs two IV lines
Draw required labs. Avoid non essential
Don’t shake the drug. It will foam.
Assess vs, neuro, cardiac rhythm q 15 min.
Check for signs of bleeding
Monitor lab values
Assess vs, neuro, cardiac rhythm q 15 min.
then q 2 hours for 24 hours
Monitor for signs of bleeding for 72 hours.
signs of reperfusion (thrombolytic therapy)
•Abrupt cessation of chest pain
•Resolution of ST elevation/depression
•Rapid rise of CK-MB
•Reperfusion dysrhythmias---generally self limiting
complications of thrombolytic therapy
•Reocclusion of the artery. May start heparin therapy to prevent this.
nitroglycerine drug therapy
•May be used short term to reduce the infarct size, decrease heart workload and increase blood supply.
•Hypotension, reflex tachycardia are side effects so BP and heart rate are monitored closely and drug is carefully titrated,
•Want to keep BP above 90 systolic and heart rate below 110.
•Given for chest pain unrelieved by nitroglycerine. Is a vasodilator so decreases cardiac workload by lowering myocardial oxygen consumption.
•Reduces contractility, BP and heart rate
•Reduces fear and anxiety
•In rare cases can depress respirations.
good thing about TPA
specific. Goes right for the clot
•Angiotensin-Converting Enzyme Inhibitors
•Angiotensin II Receptor Antagonists
•Lipid lowering drugs
nursing care for drug therapy
•Continue to monitor vs, cardiac rhythm, response to drug therapy.
•Space activities with rest
•After 48 hrs encourage gradual increase in self care activities. Monitor response to activity ie. Vs, O2 sat, changes in cardiac rhythm, chest pain.
•Decrease meal time fatigue
Small, frequent meals, no very hot or cold
foods. Sufficient time for meals
•Begin rehab teaching early
•Encourage and supervise increased activity level.
Start with lying & sitting exercises
Increase length of ambulation
Encourage exercise for 20 minutes twice a
•Teach patient to monitor pulse during exercises and to stop if pulse doesn’t increase or if it rises to 20 over resting pulse.
•Reinforce plans for home activity program