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Med Surg > Disorders of Cardiac System 2 > Flashcards

Disorders of Cardiac System 2 Flashcards

1
Q

what does hypoxia lead to

A

vasodilation of blood vessels and acidosis from the ischemia

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2
Q

Potassium, Calcium and Magnesium imbalances lead to

A

changes in conduction

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3
Q

inferior ACS pts sometimes develop what dysrhythmias

A

bradycardias & second degree AV blocks

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4
Q

anterior ACS pts sometimes develop what dysrhythmias

A

Premature ventricular contractions; third degree or bundle branch blocks are serious complications that indicate a large portion of the left ventricle is involved –may need a pacemaker

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5
Q

types of MI

A

Subendocardial- Fewer effects on wall motion and cardiac output
Transmural- Through all 3 layers of the heart muscle

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6
Q

changes after an MI

A

Changes occur 6 hours after infarction, appears blue and swollen
After 48 hours the infarcted area turns gray with yellow streaks as WBC’s invade the tissue and try to remove necrotic area
Necrotic area becomes a shrunken with firm scar tissue within 8-10 days
This changes the shape and size of the ventricle, ventricular remodelingdecreased ventricular functioning and eventual heart failure, the area does not contract nor conduct electricity

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7
Q

ECG changes to ischemia post MI

A

ST segment depression
T wave inversion
Returns to normal when ischemic episode is over
Reversible

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8
Q

ECG changes to injury post MI

A 
Prolonged, intense ischemia
ST elevation
Patient with unstable angina
Q wave abnormality 
Damage may or may not be reversed
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9
Q

ECG changes to infarct post MI

A

Death to myocardial muscle

Not reversible

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10
Q

common description of MI pain

A

Described as crushing or elephant sitting on chest

Pressure radiating to left arm and jaw

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11
Q

women describe MI pain

A

usually present with atypical s/s
GI symptoms, epigastric pains, or choking sensation
“Triad” of symptoms – indigestion, chronic fatigue, inability to catch breath

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12
Q

diabetics describe MI pain

A

those that have neuropathy may not be able to sense severity of pain

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13
Q

elderly describe MI pain

A 
are likely to present with less or NO pain
#1 sign of MI in elderly is SOB
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14
Q

describe vomiting in relation to MI

A

occurs because acute pain stimulates the vomiting center in the brain - stimulation of vagus nerve - decreased HR - decreased CO - decreased BP.
Vomiting is a BAD SIGN!

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15
Q

assessment of MI

A

ECG changes
Vomiting
Indications of decreasing cardiac output:
Cold, clammy, BP decreasing

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16
Q

what labs diagnose MI

A

Troponins T and I
CK-MB (creatine kinase)
Myoglobin

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17
Q

what tests diagnose MI

A

12 lead ECG
Cardiac Catheterization
Stress Test is non emergent

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18
Q

describe the CPK-MB lab test

A

Cardiac specific isoenzyme
Increased with damage to cardiac cells
Elevated within 3-6 hours after the onset of symptoms; peaks in 12-24 hours

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19
Q

describe troponin lab test

A

Cardiac biomarker with high specificity to myocardial damage
Elevates within 3-4 hours and remains elevated for up to 3 weeks
It is THE MOST sensitive and most specific in detecting cardiac muscle damage
***If troponin levels are elevated, there IS heart muscle damage

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20
Q

describe myoglobin lab test

A

Levels start to increase within 1 hour and peak in 12 hours after the onset of symptoms
Not specific enough to diagnose an acute coronary syndrome, BUT if it is negative, it is a great way to rule out an acute MI
Negative result on myoglobin is a GOOD thing!

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21
Q

what is important to remember about V-Fib

A

DEFIB V-FIB!!

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22
Q

what Untreated major arrhythmias can put a client at risk for sudden death following ACS

A

Pulseless V-tach
V-fib
Asystole

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23
Q

Any deviation from the normal rhythm of the heart

A

dysrhythmia

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24
Q

Used for the treatment and prevention of disturbances in cardiac rhythm

A

Antidysrhythmics

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25
Q

Common Dysrhythmias

A

Supraventricular dysrhythmias
Ventricular dysrhythmias
Ectopic foci
Conduction blocks

26
Q

System commonly used to classify antidysrhythmic drugs

Based on the electrophysiologic effect of particular drugs on the action potential

A

Vaughan Williams Classification

27
Q

class one of Vaughan Williams classification

A

Membrane-stabilizing drugs
Fast sodium channel blockers
Divided into Ia, Ib, and Ic drugs, according to effects

28
Q

class 1a of VW

A 
quinidine, procainamide, disopyramide
Block sodium (fast) channels
Delay repolarization
Increase APD
Used for atrial fibrillation, premature atrial contractions, premature ventricular contractions, ventricular tachycardia, Wolff-Parkinson-White syndrome
29
Q

class 1b of VW

A

phenytoin, lidocaine
Block sodium channels
Accelerate repolarization
Increase or decrease APD
Lidocaine is used for ventricular dysrhythmias only
Phenytoin is used for atrial and ventricular tachydysrhythmias caused by digitalis toxicity, long QT syndrome

30
Q

class 1c of VW

A

flecainide, propafenone
Block sodium channels (more pronounced effect)
Little effect on APD or repolarization
Used for severe ventricular dysrhythmias
May be used in atrial fibrillation/flutter, Wolff-Parkinson-White syndrome, supraventricular tachycardia dysrhythmias

31
Q

class 2 of VW

A

beta blockers: atenolol, esmolol, metaprolol
Reduce or block sympathetic nervous system stimulation, thus reducing transmission of impulses in the heart’s conduction system
Depress phase 4 depolarization
General myocardial depressants for both supraventricular and ventricular dysrhythmias
Also used as antianginal and antihypertensive drugs

32
Q

class 3 of VW

A

amiodarone, dronedarone, dofetilide, sotalol*, ibutilide
Increase APD
Prolong repolarization in phase 3
Used for dysrhythmias that are difficult to treat
Life-threatening ventricular tachycardia or fibrillation, atrial fibrillation or flutter that is resistant to other drugs

33
Q

class 4 of VW

A

verapamil, diltiazem
Calcium channel blockers
Inhibit slow-channel (calcium-dependent) pathways
Depress phase 4 depolarization
Reduce AV node conduction
Used for paroxysmal supraventricular tachycardia; rate control for atrial fibrillation and flutter

34
Q

describe adenosine (Adenocard)

A

Slows conduction through the AV node
Used to convert paroxysmal supraventricular tachycardia to sinus rhythm
Very short half-life—less than 10 seconds
Only administered as fast IV push
May cause asystole for a few seconds
Other adverse effects minimal

35
Q

Antidysrhythmics: Adverse Effects

A 
ALL antidysrhythmics can cause dysrhythmias!
Hypersensitivity reactions
Nausea
Vomiting
Diarrhea
Dizziness
Blurred vision
Headache
36
Q

nursing implications for antidysrhythmic drugs

A

Measure baseline BP, P, I&O, and cardiac rhythm
Measure serum potassium levels before initiating therapy
Assess for conditions that may be contraindications for use of specific drugs
Assess for potential drug interactions
Report dosing schedules and adverse effects to physician
During therapy, monitor cardiac rhythm, heart rate, BP, general well-being, skin color, temperature, heart and lung sounds
Assess plasma drug levels as indicated
Monitor for toxic effects

37
Q

Solutions of lidocaine that contain epinephrine…

A

should not be given IV—they are to be used ONLY as local anesthetics

38
Q

Ensure that the patient knows to notify health care provider of any worsening of dysrhythmia or toxic effects like…

A

Shortness of breath
Edema
Dizziness
Syncope

39
Q

Teach patients taking beta blockers, digoxin, and other drugs…

A

how to take their own radial pulse for 1 full minute, and to notify their physician if the pulse is less than 60 beats/minute before taking the next dose

40
Q

what therapeutic responses should you watch for post antidysrhythmic

A 
Decreased BP in hypertensive patients
Decreased edema
Decreased fatigue
Regular pulse rate 
Pulse rate without major irregularities
Improved regularity of rhythm
Improved cardiac output
41
Q

treatment methods of acute MI emergency

A

Relieve Pain
Decrease myocardial O2 demand
Increase myocardial O2 supply

42
Q

immediate interventions of acute MI

A 
Evaluate the pain
Get vital signs
Get IV access, what size?
Call the MD for orders
Is there a protocol, if not call RRT (rapid response team)
Provide continuous telemetry
Obtain a 12 lead ECG
Give O2 to maintain sats at 95%
Begin MONA protocol
Don’t leave the patient and family
43
Q

What is MONA?

A

morphine (2-10mg IV ), oxygen (2-4 L), nitro(0.4mg SL x 3 doses 5 min. apart), aspirin (325 mg)

44
Q

what is the new treatment recommendation of MI (not MONA)??

A

O2
Aspirin if not given before arrival at the hospital
Nitro
Morphine if pain not relieved by Nitro

45
Q

describe thrombolytics

A

tPA (tissue plasminogen activator) Alteplase and Reteplase IV or intracoronary
Give within the first 6 hours of the event
Used if unrelieved by NTG

46
Q

absolute contraindications of thrombolytics

A

Prior intracranial Hemorrhage, AV malformation, brain tumors
Ischemic stroke within 3 months
Suspected aortic dissection
Active bleeding
Closed head or facial trauma within 3 monts

47
Q

relative contraindications of thrombolytics

A 
Severe uncontrolled HTN >180 SBP or >110 DBP
CPR > 10minutes
Major surgery within 3 weeks
Pregnancy
High INR
48
Q

describe process of thrombolytic therapy

A

Ideal door to drug time is 30 mins; but can be administered within 6-8 hours after the onset of pain
If facility has Interventional radiology department client will go to cath lab instead of getting thrombolytic
Goal is to dissolve the clot that is blocking the blood flow to the heart
Decreases the size of the infarction

49
Q

important to note for thrombolytics

A

Watch for bleeding!!
Hemorhage is major concern!
Be sure to draw blood when starting the IV to minimize the number of puncture sites
NO ABGs!

50
Q

what do glycoprotein inhibitors do

A

Prevent fibrinogen from attaching to platelets
Used in ACS, nonSTEMI and non-Q wave MI
Used before and during PTCA (cardiac cath)
May be used with tPA or Heparin, but the dose is adjusted by 25-50%

51
Q

cautions with tPA and glycoproteins

A

*Monitor for bleeding at all sites
Monitor neurologic status or c/o headache
Monitor clotting status
Monitor Hgb and Hct
Monitor stool, urine and emesis for occult blood
Watch for possible allergic reactions (streptokinase most common for allergic reactions)
If the patient is less than 65 kg, the dose may need to be adjusted
**Call the MD for any signs of bleeding or confusion

52
Q

describe beta blockers given for MI

A

Metoprolol/toprol XL, carvedilol/coreg
Given to decrease the workload on the heart, decrease the extent of the infarct and prevent dysrhythmias
Given within the first 1-2 hours after and MI

53
Q

describe when ACE inhibitors given for MI

A

after beta blockers given

Given with 48 hours to prevent ventricular remodeling (scar tissue) and heart failure

54
Q

describe medical interventions for MI other than drugs

A

Percutaneous Coronary Intervention: Includes all interventions such as angioplasty and stents
Implemented to try and open up the coronary artery to restore blood flow to the heart
Goal time is to perform within 90 mins of MI
Major complication is a MI
Chest pain after the procedure may indicate re-occluding and client needs to go back to cath lab! Call HCP ASAP

55
Q

percutaneous coronary interventions

A 
Clients will be on thrombolytic or anti-platelet medications such as:
Aspirin
Clopidogrel
Abciximab (ReoPro IV)
Eptifibatide (Integrilin)
56
Q 
Smoking cessation
Increase activity gradually
No isometric exercises
No valsalva/no straining for BMs
Diet: 
Low fat, low salt, low cholesterol
Shop the perimeter of the grocery store!
A

Cardiac Rehabilitation Plan

57
Q

sex in relation to cardiac rehabilitation

A 
Sex can be resumed when client can walk around the block or up a flight of stairs with no discomfort
Patients who do not have any complications can resume sexual activity within 1 week to 10 days following MI onset and treatment
Morning time (safest time of day) when the client is well rested
58
Q

s/s of heart failure

A

Weight gain
Ankle edema
SOB and confusion

59
Q

what is the best exercise for MI client

A

walking

60
Q

complications following an MI

A

Dysrhythmias
Leading cause of hospital death in MI patients
How do you control for these??
Heart failure- discussed later
Left ventricular failure and cardiogenic shock- discussed in critical care lecture
CABG (coronary artery bypass graft)- in critical care lecture
Psychological Responses: Denial, Depression, Role change

61
Q

treatment following MI

A

Lifestyle modifications:
Cardiac rehab, smoking cessation, wt. control, control of
BP < 140/90, control of diabetes, FBS 80-100
Pharmacological management:
Lipid lowering agents
Anti-platelets (clopidogrel or prasugrel) (plavix & effient) Nitrates if angina
Aspirin
Beta blockers
Placement of ICD 40 days after MI if ejection fraction remains <35%

62
Q

expected pt outcomes following MI

A

Adherence to treatment plan
Improved activity tolerance
Physical comfort
Patient seeks health information
Patient describes strategies to maximize health
Modifiable risk factors will be minimized or eliminated
Angina not present

Med Surg (23 decks)

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