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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
Common Dysrhythmias
Supraventricular dysrhythmias Ventricular dysrhythmias Ectopic foci Conduction blocks
26
System commonly used to classify antidysrhythmic drugs | Based on the electrophysiologic effect of particular drugs on the action potential
Vaughan Williams Classification
27
class one of Vaughan Williams classification
Membrane-stabilizing drugs Fast sodium channel blockers Divided into Ia, Ib, and Ic drugs, according to effects
28
class 1a of VW
``` 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
class 1b of VW
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
class 1c of VW
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
class 2 of VW
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
class 3 of VW
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
class 4 of VW
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
describe adenosine (Adenocard)
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
Antidysrhythmics: Adverse Effects
``` ALL antidysrhythmics can cause dysrhythmias! Hypersensitivity reactions Nausea Vomiting Diarrhea Dizziness Blurred vision Headache ```
36
nursing implications for antidysrhythmic drugs
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
Solutions of lidocaine that contain epinephrine...
should not be given IV—they are to be used ONLY as local anesthetics
38
Ensure that the patient knows to notify health care provider of any worsening of dysrhythmia or toxic effects like...
Shortness of breath Edema Dizziness Syncope
39
Teach patients taking beta blockers, digoxin, and other drugs...
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
what therapeutic responses should you watch for post antidysrhythmic
``` 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
treatment methods of acute MI emergency
Relieve Pain Decrease myocardial O2 demand Increase myocardial O2 supply
42
immediate interventions of acute MI
``` 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
What is MONA?
morphine (2-10mg IV ), oxygen (2-4 L), nitro(0.4mg SL x 3 doses 5 min. apart), aspirin (325 mg)
44
what is the new treatment recommendation of MI (not MONA)??
O2 Aspirin if not given before arrival at the hospital Nitro Morphine if pain not relieved by Nitro
45
describe thrombolytics
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
absolute contraindications of thrombolytics
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
relative contraindications of thrombolytics
``` Severe uncontrolled HTN >180 SBP or >110 DBP CPR > 10minutes Major surgery within 3 weeks Pregnancy High INR ```
48
describe process of thrombolytic therapy
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
important to note for thrombolytics
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
what do glycoprotein inhibitors do
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
cautions with tPA and glycoproteins
*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
describe beta blockers given for MI
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
describe when ACE inhibitors given for MI
after beta blockers given | Given with 48 hours to prevent ventricular remodeling (scar tissue) and heart failure
54
describe medical interventions for MI other than drugs
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
percutaneous coronary interventions
``` Clients will be on thrombolytic or anti-platelet medications such as: Aspirin Clopidogrel Abciximab (ReoPro IV) Eptifibatide (Integrilin) ```
56
``` 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! ```
Cardiac Rehabilitation Plan
57
sex in relation to cardiac rehabilitation
``` 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
s/s of heart failure
Weight gain Ankle edema SOB and confusion
59
what is the best exercise for MI client
walking
60
complications following an MI
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
treatment following MI
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
expected pt outcomes following MI
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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