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exam 2 > cardiology > Flashcards

cardiology Flashcards

1
Q

what must a doctor do before putting a patient on quinadine

A

they need to digitilize the person first because the dig takes care of the heart rate.

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2
Q

quinidine

A

exacabates CHF

causes thrombocyteapenia

extends refractory period

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3
Q

Norpace side effects

A

dry mouth

exacabates CHF

urinary retention

thrombocytopenia

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4
Q

Lidocaine for the heart

A

has to be preservative free (No epinephrine)

makes it harder for a patient to go into a v fib

treats pvc’s

prevents patient from going into v tach

anestasizes the heart

0.5-1 mg/kg depending on your person

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5
Q

lidocaine IV can cause

A

causes seizures

push over 1-2 minutes (preferably 2 minutes)

can cause confusion (especially in elderly)

can get a psychosis

cardiovascular hypotension

bradycardia

possible blocks and arrests

other arrthymias

double vision

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6
Q

important about lidocaine

A

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

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7
Q

class 1 C drugs.

A

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.

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8
Q

class 1 c drugs

A

Agents:

. Flecainide (Tambacor)

. Propafenone hydrochloride ( Rythmol )

Action:

. Most potent Class I agents. Slows conduction through atria , purkingee

 system and ventricals.  Decreases repolarization rate.  Decreases contractility.

. Causes decrease in PVCS and VT

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9
Q

class 2 Beta blockers

A

Action:

. 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.

Agents:

. Propranolol ( Inderal )—non selective

. Metoprolol ( Lopressor )—selective

. Atenolol ( Tenormin )

. Sotalol ( Betapace )

Adverse effects:

. 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

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10
Q

negative inotropic effect causes

A

heart failure

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11
Q

dromotropic effect causes

A

(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

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12
Q

inotropic effect

A

(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

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13
Q

chronotropic effect

A

(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

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14
Q

interactions with Beta Blockers

A

. 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.

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15
Q

nursing considerations for Beta Blockers

A

. 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.
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16
Q

potassium channel blockers

A

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 )
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17
Q

potassium channel blockers

A

ex. AMIODARONE

Use:

. 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.
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18
Q

contraindications of potassium channel blockers

A

. 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.
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19
Q

precautions for potassium channel blockers

A

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

                bluish color
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20
Q

nursing considerations for potassium channel blockers

A

. 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

  constipation.

. Missed dose: Omit. Do not double up on missed dose. Notify MD if two or

   more doses are missed.
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21
Q

covert

A

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.

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22
Q

class 1 sodium channel blockers

A

. Decrease rate of conduction

. Prolongs action potential duration

. Reduces speed of impulse conduction

. For atrial and ventricular dysrhythmias

CLASS Ia

AGENTS

. Procainamide ( Pronestyl )

. Disopyramide ( Norpace )

. Quinidine ( Quinidex )

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23
Q

indications of sodium channel blockers

A

ex: PROCAINAMIDE (PRONESTYL )

Indications:

Ventricular arrhythmias

  .  Stable ventricular tachycardia

  .  Premature ventricular contractions

  .  Ventricular fibrillation

Supraventricular tachyarrhythmias

  .   PSVT,  PAT,  Junctional tachs. , 

  .   Atrial flutter and fibrillation
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24
Q

actions of sodium channel blockers

A

. 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.

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25
Q

adverse effects of sodium channel blockers

A

Adverse effects:

  .  Myocardial depression.  Prolongs duration of QRS, QT interval, AV           

     conduction.

  .  Hypersensitivity.  Confusion, seizures, dizziness.

. Hypotension if given too fast IV. Blood dyscrasias like thrombocytopenia.

. Gastric: anorexia, diarrhea, nausea, vomiting.

Nursing:

. 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.
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26
Q

QUINIDINE (QUINIDEX)

A

action:

. Slows conduction through cardiac tissue. Refractory period is lengthened

   especially in atria.  Used for atrial flutter or fibrillation to maintain sinus

   rhythm.

. 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.

Dosage:

. 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

Adverse Effects:

. 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.

Interactions:

. Will increase digoxin levels. Nifedipine will decrease Quinidine levels.

Nursing:

. 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.

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27
Q

DISOPYRAMIDE ( NORPACE )

A

Action:

. Prolongs refractory period. Decreases myocardial contractility. Has

  anticholinergic effect so patients with A. Flutter and A. Fibrillation

  should be digitalized first.

Adverse effects:

. 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

. Thrompocytopenia

. Renal: Urinary retention, hesitancy,and frequency

. Endocrine: Hypoglycemia

. Rash

Nursing:

. 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.

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28
Q

class 1 b drugs

A

Agents:

. Lidocaine (Xylocaine)

. Tocainide ( Tonocard)

. Mexiletine ( Mexitil)

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29
Q

LIDOCAINE ( XYLOCAINE )

A

Action:

. Elevates ventricular fibrillation threshold

. Treats symptomatic PVCS. Suppresses ventricular tachycardia.

Dosage:

. 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

Adverse effects:

. CNS: Paresthesias, numbness, agitation, confusion, seizures.

. CV: Hypotension, bradycardia, cardiac arrest, arrhythmias

. GI: vomiting

. Integ: Phlebitis

Nursing;

. Monitor vital signs, EKG, QRS and QT levels

                                                          (3)

. Monitor serum levels. Signs of toxicity include confusion, excitation, blurred

 or double vision, nausea, vomiting, tinnitus, tremors, convulsions, difficulty

  breathing.

. 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.

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30
Q

calcium channel blockers (class IV)

A

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

Agents:

. Ditiazem ( Cardizem )

. Verapamil ( Calan )

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31
Q

DILTIAZEM ( CARDIZEM )

A

Use:

. 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

Contraindications:

. Hypersensitivity, sick sinus syndrome, 2nd or 3rd Heart , severe hypotension ( less

    than 90/60 ).  Patients undergoing cranial surgery, bleeding aneurysms

Caution:

. CHF especially if on beta blocker. Conduction abnormalities. Renal or

 hepatic impairment

Dose:

. 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

 infusion

. PO—usual dose 180 to 360 mg/day in divided doses or 60 to 120 mg

 sustained release

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,

         increased weight.

.Skin rash

Drug Interactions:

. Increases digoxin levels. Additive effects on AV conduction with beta blocker.

. Cimetidine can increase cardizem levels

Nursing:

. 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.
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32
Q

VERAPAMIL ( CALAN )

A

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

  30 minutes

Interactions:

. Beta blockers increase risk of CHF, bradycardia,heart block

. Increases digoxin levels.

. Lithium and cyclospore may be increased to toxic levels.

Nursing:

. 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.

                                                (7)

. Same as with cardizem

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33
Q

ADENOSINE ( ADENOCARD )

A

Action:

. Slows impulse formation in SA node. Slows conduction time through AV node.

  Depresses left ventricular function and restores NSR.

. General cardiac depressant

Uses:

. Paroxysmal supraventricular tachycardia

Precautions:

. Sick sinus syndrome may be worsened by drug and produce sinus arrest

Dosage:

. 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

Side Effects:

. Arrhythmias , flushing, heart block, chest pain, SOB, cough, dizziness ,

  numbness, tingling in arms.

Nursing:

. Continuous EKG. Monitor BP and pulse, lung sounds, respiratory

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34
Q

ATROPINE SULFATE

A

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.

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35
Q

inotropic

A

force of contraction

positive inotropic increases the force

negative inotropic decreases the force

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36
Q

dromotropic

A

conduction pattern

negative dromotropic slows conduction

positive dromotropic speeds up contraction

conduction goes from arrythmia to heart block

37
Q

Chronotropic

A

heart rate (can go both ways)

positive chronotropic speeds up heart rate

negative chronotropic slows down heart rate

38
Q

negative inotropic

A

if contraction not forceful enough blood backs up causing heart failure

39
Q

when starting a drip

A

know baseline QT interval

40
Q

if there is 50% or more distance between 2 complexes

A

may be a block

41
Q

cardioversion

A

used for every rhythm that has a T wave

42
Q

defribilization

A

only for v fib (only only only)

before you shock someone yell all clear and make sure you are not touching the patient

43
Q

sodium channel blockers

A

stabilize membranes

decreases irritation

decreases etopic beats from starting

44
Q

beta 2

A

lungs

45
Q

beta 1

A

heart

46
Q

lopresser IV

A

5mg (3 bolus’) then PO

47
Q

if adenosine doesnt work

A

cardiovert

48
Q

anatomy and physiology of an MI

A

. Sudden blockage of one of the branches of

       the coronary arteries.  When blood flow

       acutely decreases by 80% to 90% ischemia

       develops.

 b.  If blood flow is not restored myocardial

      tissue necrosis can happen over a period

      of hours.
49
Q

what rhythm are patients usually in with an M.I.

A

V. Fib

50
Q

M.I. anatomy and physiology

A

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

       emboli.

  e.  Cardiac cells can withstand ischemia

        about 20 minutes before injury occurs.
51
Q

during an M.I.

A

Within 4 to 6 hours the entire thickness of

     the heart will become necrotic.
52
Q

Around the area of infarction there are

      two zones:
A

.

               Zone of Injury

           Zone of ischemia
53
Q

necrotic tissue is

A

electrically inert

54
Q

zone of ischemia

A

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

55
Q

acute coronary syndrome

A
  • 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.
56
Q

pathology of an MI

A
  • 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.
57
Q

promestyl

A

iv bolus

give Over 5 minutes

if too fast causes seizures, blocks, hypotension

58
Q

anterior wall MI

A

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

     MIs.

d.  EKG shows ST elevations, abnormal Q waves.
59
Q

inferior wall MI

A

right sided

Results from occlusion of right coronary

     artery.  Is 17% of all MIs.  10% mortality

     rate.

b.  About 1/3 have right ventricular MI and

     right ventricular failure.

c.  EKG can show ST and T wave changes and

     Q waves.

(T wave inverts, thats NOT NORmal)

60
Q

posterior and lateral wall MI’s

A

least complications

•Result from obstruction of the circumflex

artery.
  • Posterior MI is 2% all MIs. Is uncommon.
  • Lateral wall MIs have the least complications.
61
Q

gender differences in acute coronary syndrome

(Men)

A

Men are developing CAD at a younger age

     than women and their death rates are

     declining.

b.  Initial cardiac event is more often MI than

     angina.

c.  Have higher rate of left ventricular

     hypertrophy.

d.  Have greater collateral circulation.
62
Q

gender differences in acute coronary syndrome

(Women)

A

CAD causes more deaths in women than

     men.  Usually older and sicker with first

     MI. 

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

     than men.

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.
63
Q

gerontologic considerations with an MI

A
  • 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.
64
Q

cultural and ethnic consideration for MI’s

A
  • 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.
65
Q

Risk Factors for CAD

A

•Non Modifiable:

Age

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

Smoking

Physical inactivity

Obesity: waist circumference greater than 39.8 in men & 34.3 in women.

•Contributing factors:

Diabetes Mellitus

Fasting blood sugar > 110 mg/di

Psychologic states

Homocysteine levels-if elevated can contribute to atherosclerosis

66
Q

stages of MI healing

A

•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

from dysrhythmias.

67
Q

stages of MI healing

A

•4th to 7th day:

Softening of infarct area. Danger of

aneurysm formation.

•8th to 10th day:

Newly formed capillaries develop around

infarct but it is 2 to 3 weeks before any

significant circulation.

68
Q

stages of MI healing

A

•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

maximum strength.

69
Q

clinical manifestations of an MI

A
  • 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
70
Q

Deviations in the manifestations of an MI

A
  • 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.
71
Q

diagnostic evaluation

A
  • Electrocardiogram-serial readings to monitor evolution of MI.
  • Troponin Levels-establishes diagnosis of MI.
  • Cardiac Enzymes-CK (Creatine Kinase).
  • Isoenzymes:CK-MB-Heart
  • Myoglobulin
  • 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.
72
Q

with an MI the

A

st segment elevates

T wave inversion

73
Q

with ischemia of the heart

A

st segment depression

T wave inversion

74
Q

what meds do they hold for Heart tests

A

usually beta blockers

75
Q

goals for med management of MI

A
  • Minimize myocardial damage, relieve pain & provide rest
  • Prevent complications
76
Q

emergency management of an MI

A
  • 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.
77
Q

ongoing monitoring of an MI

A
  • 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.
78
Q

thrombolytic therapy

A
  • 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.
79
Q

Thrombolytic side effects/adverse reactions

A
  • Hemorrhage and anemia
  • Hypotension, fever
  • Bronchospasm, anaphylaxis
  • Periorbital swelling, itching, urticaria, headache
  • Reperfusion dsyrhythmias
80
Q

contraindications for thrombolytic therapy

A

•Absolute:

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

Aortic dissection

•Relative Contraindications:

Active peptic ulcer disease

Current use of anticoagulants

Pregnancy

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

Prolonged CPR

Patients who weigh less than 65 kg have to

dose adjusted because of increased

likelihood of bleeding.

81
Q

nursing implications of thrombolytic therapy

A

•Prior to treatment:

Assess vs, neuro, and cardiac rhythm.

Patient needs two IV lines

Draw required labs. Avoid non essential

punctures.

Don’t shake the drug. It will foam.

•During treatment:

Assess vs, neuro, cardiac rhythm q 15 min.

Check for signs of bleeding

Monitor lab values

•After treatment:

Assess vs, neuro, cardiac rhythm q 15 min.

then q 2 hours for 24 hours

Monitor for signs of bleeding for 72 hours.

82
Q

signs of reperfusion (thrombolytic therapy)

A
  • Abrupt cessation of chest pain
  • Resolution of ST elevation/depression
  • Rapid rise of CK-MB
  • Reperfusion dysrhythmias—generally self limiting
83
Q

complications of thrombolytic therapy

A
  • Reocclusion of the artery. May start heparin therapy to prevent this.
  • Bleeding
84
Q

nitroglycerine drug therapy

A
  • 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.
85
Q

morphine sulfate

A
  • 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.
86
Q

good thing about TPA

A

specific. Goes right for the clot

87
Q

Drug therapy

A
  • Beta blockers
  • Angiotensin-Converting Enzyme Inhibitors
  • Angiotensin II Receptor Antagonists
  • Aspirin
  • Anticoagulants
  • Antidysrhythmic drugs
  • Stool Softners
  • Lipid lowering drugs
88
Q

nursing care for drug therapy

A
  • 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 exercisesIncrease length of ambulationEncourage exercise for 20 minutes twice aday.
  • 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

exam 2 (9 decks)

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