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110_Cardiac > Mid Term 1_RegNrsng 110 _Cardiac > Flashcards

Mid Term 1_RegNrsng 110 _Cardiac Flashcards

1
Q

Verpamil pt. teaching, furosemide, SVT treatment, pedal pulses before and after surgery, pt. with chest pain 1st drug to be given,

A
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2
Q

Cardiac Tamponade wrap-up

A
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3
Q

Cardiac Tamponade
Def:
Low oxygen signs = hypoxia = LOC = huge test tip here = change in mental status. = Dizziness and passing out called syncope and SOB / dyspnea.
Tachycardia which is the very first sign of decreased cardiac output.

A

Hemodynamic monitoring is only heard after a big tube is placed inside the heart. This big tube is called swanz- guanz = measures the CVP for critically ill patients.

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4
Q

Endocarditis vs Pericarditis wrap up

A
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5
Q

Endocarditis
Cause:
step throat, dental visit, valve replacement surgery, IV drugs & dirty needles, hx of heart problems

A

Most deadly complication
stroke (CVA) break off of clot.
Assess for change in LOC

Confusion, agitation, slurred speech weakness, and facial drooping (last sign) – signs of IE

s/s: Janeway lesion are flat circular lesions on the palms and soles of the feet. Janeway looks like burn marks.
Painful osler’s nodes

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6
Q

Pericarditis

Cause:
MI, viral infection - HIV, TB, Herpes; heart attack, renal failure (uremia - high BUN), autoimmune d/o - lupus, RA.

Others: Chest Trauma, Radiation Therapy, Phenytoin, Hypothyroidism

A

s/s Pericarditis:

ST elevation
A-fib
Elevated WBC (over 10,000). Fever
Elevated C-Reactive Protein
Pericardial Friction Rub
Precordial Chest Pain
Fatigue, Dysphagia
Elevated BUN and Cr

Monitor Pulses Paradoxes - drop in SBP by 10 mmHg.

Pt. Care: Tripod/ High Fowler position, Oxygen, Pain

Tx: Pericardiocentesis

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7
Q

Cardiac Meds HF

ACE and ARBS

A

Both ACE and ARBS blocks the RAAS that retains water.
Retains potassium and lets water and sodium go out.

ACE inhibitors side effects = angioedema = prils puff up the tongue and not SARTANS.
C = cough - Only PRILS do that
E= elevated potassium
ACE avoid for pregnancy

With prils and SARTANS avoid potassium rich food = green leafy veggies and fruits, and liver.

*Cardiac momitor with BP

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8
Q

Cardiac Meds:

*Safe admin of IV Lasix, frequency and effectiveness.
Diuretics:
Butenamide, Furosemide

Lasix Administration:
Adults administration rate not to exceed 4 mg/min to prevent ototoxicity. Concentration of IV med = 1mg/mL

(Peds: not to exceed 1 mg/kg/min)

PO Med: 20 -40 mg twice a day, not to exceed 80 mg

A

Furosemide too fast causes:
Ototoxicity, Hypotension

Too much Lasix for long term causes: Nephrotoxicity, Hypokalemia

Hold diuretics for: Low BP, high BUN & Creatinine, low potassium

Give at morning, slow position changes, daily weights, low sodium diet, sunburn

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9
Q

Verapamil and its health teaching
Calcium channel blockers exception : Nifedipine can be given for low HR. As it only affects the BP.

A

Nursing Considerations:
*Hold drug for SBP < 100, HR < 60 BPM,
* Notify HCP for irregular heart beats, rash, dyspnea, swelling of hands and feet, dizziness, nausea, constipation, or hypotension, and if HA is severe or persistent.
* Hypotensive / drowsiness/ dizziness - slow position changes/ avoid driving
* Headache is common SE.
* Do not take with Nitro/ Beta-blockers
* Photosensitivity / sunscreen
* good dental hygiene -

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10
Q

Anticoagulants, such as heparin or warfarin (also called Coumadin), slow down your body’s process of making clots.

*anticoagulant = hospital = used to prevent clots, but do not dissolve clots

A

Antiplatelets, such as aspirin and clopidogrel, prevent blood cells called platelets from clumping together to form a clot. Antiplatelets are mainly taken by people who have had a heart attack or stroke

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11
Q

Pt. teaching anticoagulant and antiplatelets

A

Watch for signs of bleeding like bleeding gums, hematauria, hematemesis - couging up blood, bruising, hematomas, injury prevention - no contact sports

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12
Q

Lab
aPTT = 30 -40 sec
Heparin aPTT = 45 - 80 sec

PT= 11 -13 sec
Warfarin PT = 17 -26 sec

INR = 0.8 -1.1
Warfarin INR = 2-3

Plt = 150,000 to 450,000 platelets per microliter

A

D- Dimer detecting blood clots like in Pul Embolism < 0.4 mcg/ mL

BNP < 100 pg/ mL
HP > 100

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13
Q

Valvular stenosis
not enough blood goes through- narrowin of valve

A

Regurgitation
valve does not close effectively and blood is backed up

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14
Q

Mitral Valve Stenosis result from

A

Rheumatic Heart disease

Clinical Manifectations:
Exertional dyspnea r/t dec. lung compliance
Loud S1
Murmur
Fatigue
Palpitations
Hoarseness, hemoptysis
Chest pain, seizures/stroke

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15
Q

Mitral Valve Regurgitation cause

  • Drug for MR = Beta - Blockers.
A

MI
IE
Chronic rheumatic heart disease
Mitral valve prolapse
Ischemic papillary muscle dysfunction

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16
Q

Mitral Valve Regurgitation results in

A

Pulmonary Edema,
Left Artrial Enlargement, Ventricular Hypertrophy, decreased CO

clinical manifestations:
thready, peripheral pulses and cool, clammy extremities

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17
Q

Most common form of valvular disease in the US

A

Mitral Valve Prolapse

a murmur from regurgitation that is louder during systole.

Manifestations:
dysrhythmias can cause palpitations, light-headedness, and dizziness

Infective endocarditis (ass. w/ MVP)
Chest pain unresponsive to nitrates

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18
Q

RN teaching MVP (Mitral Valve Prolapse)

A

Antibiotic prophylaxis before dental work or invasive procedures if MR present
Take drugs as prescribed
Healthy diet; avoid caffeine
Avoid OTC stimulants
Exercise
When to call health care provider

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19
Q

Aortic Stenosis
In older adults caused by Rheumatic Fever.

Clinical Manifestations AS:
classic triad of angina, syncope, and exertional dyspnea,
*Systolic murmur, * prominent S4

A

Aortic Stenosis results in
- Left ventricular hypertrophy and ↑ myocardial oxygen consumption
- Leads to ↓ CO, pulmonary hypertension, and HF

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20
Q

Aortic Stenosis
= Systolic Murmur

A

Aortic Regurgitation = water-hammer pulse (a strong, quick beat that collapses immediately).

diastolic murmur, S3 or S4 sound
dyspnea, orthopnea, paroxysmal dyspnea, angina, cardiogenic shock = life threatening.

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21
Q

Tricuspid valve stenosis

A

occurs primarily in pts w/ rheumatic fever or abuse IV drugs

Right atrial enlargement and
↑ systemic venous pressure
Clinical manifestations
Peripheral edema
Ascites
Hepatomegaly
Murmur

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22
Q

Pulmonic Valve Stenosis

A

Almost always congenital
Causes right ventricular hypertension and hypertrophy
Clinical manifestations
Fatigue
Loud murmur

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23
Q

Dx for valvular heart disease
- Patient’s history/physical exam
- CT scan of chest
- Echocardiogram
- Chest x-ray
- ECG
- Cardiac catheterization

A

Conservative management of valvular heart disease:

Prophylactic antibiotic therapy to prevent recurrent RF and IE
Prevent exacerbations of HF, pulmonary edema, thromboembolism

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24
Q

afib is associated with

A

Mitral Valve Regurgitation.

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25
Q

A procedure that is generally indicated for older adults and for those who are poor surgery candidates

A

Percutaneous Transluminal Balloon Valvuloplasty

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26
Q

Main complication of Mechanical Valve is

A

bleeding from the use of anticoagulants.

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27
Q

The procedure of choice for patients with pure mitral stenosis

A

Mitral commissurotomy

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28
Q

When performing a focused physical assessment for the valvular disorders which clinical manifestations should you watch for?

A
  • Fever
  • Diaphoresis, flushing, cyanosis, clubbing; peripheral edema
  • Crackles, wheezes, hoarseness
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29
Q

Overall goal of pt. with valvular heart disease is

A

(1) normal cardiac function, (2) improved activity tolerance, and (3) an understanding of the disease process and health maintenance measures.

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30
Q

Exam:
Different methods of calculating heart rate on a regular rhythms

Small Box method:

A
  • 6-sec strip method: Number of QRS complexes in 6 seconds and multiply by 10

*Small Box Method: Number of small squares between one R-R interval, and divide this number into 1500
eg: 1500/12 = 125 BPM (where R-R interval has 12 tiny boxes)

*Big Box Method: Number of large squares between one R-R interval, and divide this number into 300
eg: R-R big box = 5, then 300/5 = 60 BPM

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31
Q

Exam:
6-sec strip method, example:

A

HR = 50 BPM

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32
Q

Exam:
Measuring PQRST wave forms

A

*P-R interval = 0.12 - 0.20 (3-5 tiny boxes)
*QRS interval = 0.04-0.12 (2-3 tiny boxes)
*Q-T interval = 0.36 - 0.44 (9-11 tiny boxes)

  • each tiny box = 0.04 sec
    and big box = 0.2 sec
    then 5 bog boxes = 1 sec
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33
Q

Quick Run 9 strips

A
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34
Q

SNR

A
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35
Q

NCLEX: Bradycardia

A
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36
Q

Vfib

A
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37
Q

VTach

A
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38
Q

Note for VTach
Cardiovert vs. Defib

A
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39
Q

Afib

A
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40
Q

A-Flutter
*Aflutter similar to Afib causes and treatment. Just remember saw tooth for atrial flutter.

A
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41
Q

SVT

A
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42
Q

SVT note

A
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43
Q

Torsades de Pointe

A
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44
Q

Asystole

A
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45
Q

Key Terms

A
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46
Q

Note some stuff
Ischemia: ST depression, T wave inversion
Injury: ST elevation
Infarction: Q wave and ST elevation

A
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47
Q

Exam: Pulse Pressure

A

SBP - DBP
Example: If your blood pressure was 120/80 mmHg, that would be 120 - 80 = 40.

Risks:
*Pulse pressures of 50 mmHg or more can increase your risk of heart disease, heart rhythm disorders, stroke and more. Higher pulse pressures are also thought to play a role in eye and kidney damage from diseases like diabetes.

*Low pulse pressure — is where your pulse pressure is one-fourth or less of your systolic pressure (the top number). This happens when your heart isn’t pumping enough blood, which is seen in heart failure and certain heart valve diseases. It also happens when a person has been injured and lost a lot of blood or is bleeding internally.

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48
Q

Defib vs Cardiovert

A
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49
Q

Cardioversion for

A

Afib, Aflutter, SVT, V-Tach with pulse

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50
Q

Defibrillation for

A

V-Fib, and V-Tach without pulse

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51
Q

Afib

Fibrillation is like flopping like a fish like wave

-Most common dysrhythmia
-Prevalence increases with age
-Usually occurs in patients with underlying heart disease

A

Atrial HR = 350 -600 BPM
Ventricular HR = Variable

Atrial Rhythm: IRRegular
Ventricular Rhythm: IrRegular

P wave: Absent “fib waves” i.e. lots of little bumps between QRS complexes.

PR interval: N/A

QRS complex: Uniform appearance, duration < 0.12 sec (3 tiny boxes)

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52
Q

Afib treatment

*Afib causes a decreased CO, and an increased risk of stroke.

A

Afib Treatment
Drugs to control ventricular response, prevent stroke, and/or convert to sinus rhythm (Amiodarone most common)
*Anticoagulation

*Electrical cardioversion
*Radiofrequency ablation
*Maze procedure with cryoablation

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53
Q

A flutter

Saw teeth, no P waves here. Its like jagged saw teeth.

Causes and risks
*Typically associated with disease
* decrease CO; can cause heart failure
*Increases risk of stroke

A

Atrial HR = 250 -400 BPM
Ventricular HR = Variable

Atrial Rhythm: Regular
Ventricular Rhythm: Regular

P wave: Absen. Instead, multiple “sawtooth” flutter waves before each QRS complex

PR interval: N/A

QRS complex: Uniform appearance, duration < 0.12 sec (3 tiny boxes)

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54
Q

A flutter treatment

A

Treatment
*Pharmacologic agent
*Electrical cardioversion
*Radiofrequency ablation

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55
Q

v-fib

Ventricular fibrillation = V-fib= squiggly line = like flopping fish.

*Most deadly: V-fib, and V-tach causes SCD (Sudden Cardiac Death)

A

-Associated with MI, ischemia, disease states, procedures
-Unresponsive, pulseless, and apneic
-If not treated rapidly, death will result
Treatment:
-Treat with immediate CPR and ACLS:
Defibrillation - V-fib we always defib to save the client.
Drug therapy (epinephrine, vasopressin)

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56
Q

A patient in the coronary care unit develops ventricular fibrillation. The first action the nurse should take is to

A. Perform defibrillation. (this would be the second step because this is not usually in the room)
B. Initiate cardiopulmonary resuscitation.
C. Prepare for synchronized cardioversion.
D. Administer IV antidysrhythmic drugs per protocol.

A

B. Initiate cardiopulmonary resuscitation

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57
Q

v-tach
Ventricular tachycardia
= v-tach = tachycardic tomb stones.

*Considered life-threatening because of decreased CO and the possibility of development to ventricular fibrillation

A

Cause:
Associated with heart disease, long QT syndrome, electrolyte imbalances, drug toxicity, CNS disorders

-Can be stable (patient has a pulse) or unstable (pulseless)
-Sustained VT causes severe decrease in CO:
Hypotension, pulmonary edema, decreased cerebral blood flow, cardiopulmonary arrest

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58
Q

V-tach treatment

A

Precipitating causes must be identified and treated (e.g., hypoxia)
VT with pulse (stable) treated with antidysrhythmics or cardioversion
Pulseless VT treated with CPR and rapid defibrillation

*V-tach *with pulse we cardiovert = we hit the synchronize button.

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59
Q

SVT
SupraVentricular Tachycardia

Associated with overexertion, stress, deep inspiration, stimulants, disease, digitalis toxicity

(Reentrant phenomenon: PAC triggers a run of repeated premature beats)

A

Manifestations
HR is 151 to 220 beats/min
HR greater than 180 leads to decreased cardiac output and stroke volume
Hypotension
Palpitations
Dyspnea
Angina

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60
Q

SVT Treatment

A

Treatment
*Vagal stimulation
*IV adenosine
*IV β-blockers
*Calcium channel blockers
*Synchronized cardioversion

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61
Q

Sinus Rhythm Reading
Normal sinus rhythm
Evenly spaced apart like choo-choo trains.

A

HR = 60 -100 BPM

Atrial Rhythm: Regular
Ventricular Rhythm: Regular

P wave: Present, uniform appearance, 1 P wave per QRS complex.

PR interval: 0.12 - 0.20 secs (3-5 tiny boxes)
QRS complex: Uniform appearance, duration < 0.12 sec (3 tiny boxes)

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62
Q

Sinus Tach

Causes:
Physical activity, anxiety, stress, pain, hyperthyroidism, fever, anemia, hypoxemia, medications

A

Symptoms:
SOB, dyspnea, weakness, hypotension, chest pain, palpitations. *Angina in patients with CAD

*Patients may also be asymptomatic

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63
Q

Sinus Tach treatment

Treatment:
Guided by cause (e.g., treat pain)
Vagal maneuver
β-blockers, adenosine, or calcium channel blockers
Synchronized cardioversion

Electrical:
Cardioversion

A

Pharmaceutical Interventions:
Antiarrhythmics:
Class I: Procainamide, lidocaine
Class II: Propranolol, metoprolol, atenolol
Class III: Amiodarone, sotalol
Class IV: Verapamil, diltiazem
Class V: Adenosine, digoxin, Mag Sulfacte

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64
Q

Torsade de pointe
Tornado inside the heart. We give mag sulfate.

A
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65
Q

Sinus Brady
Causes:
Heart Block,
Hypothyroidism,
valsalva mameuvers (ex: bearing dowb), excess vagal stimulation (gagging, vomiting),
medications, electrolye imbalances, cardiovascualr diseases/ infection

A

SNB Manifestations
Hypotension
Pale, cool skin
Weakness
Angina
Dizziness or syncope
Confusion or disorientation
Shortness of breath

*Patients may also be asymptomatic

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66
Q

Sinus Brady Treatment

A

Treatment
Stop offending drugs
IV Atropine
Dopamine or epinephrine infusion
Pacemaker

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67
Q

A patient’s cardiac rhythm is sinus bradycardia with a heart rate of 34 beats/min. If the bradycardia is symptomatic, the nurse would expect the patient to exhibit:
a.Palpitations.
b.Hypertension.
c.Warm, flushed skin.
d.Shortness of breath.

A

Answer: D
Rationale: Signs of symptomatic bradycardia include pale, cool skin; hypotension; weakness; angina; dizziness or syncope; confusion or disorientation; and shortness of breath.

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68
Q

HEART BLOCK ULTIMATE GUIDE

A
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69
Q

Difference between type-2 Heart Block Mobitz II vs. 3rd degree Heart Block

A
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70
Q

1st deg Heart Block (AV Blocks)

Causes:
Associated with increasing age, disease states, and certain drugs
Usually not serious
Patients asymptomatic
No treatment
Monitor for changes in heart rhythm

A

Treatment * Not typically required. Can progress to severe type.

PR interval: Prolonged >0.20 or greater than 5 boxes.

Heart Rate: 60 -100 BPM
Atrial Rhythm: Regular
Ventricular Rhythm: Regular
P wave: Present, consistent in appearance, one P wave with each QRS complex

QRS complex: unifrom appearance, duration < 0.12 secs

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71
Q

2nd deg Heart Block (AV Blocks)
Type 1 - Mobitz I or Wenckebach

Causes:
May result from drugs or CAD
Typically associated with ischemia
Usually transient and well tolerated
*Treat if symptomatic
+Atropine
+Pacemaker
If asymptomatic, observe closely

A
  • 2nd deg type 1 AV block is usually temporary and does not require treatment. If CO is insufficient, atropine can be used. (A 2nd degree type 1 AV Block - impulse conduction progressively increases between atria and ventricles, until one impulse fails to conduct. )

PR interval: Variable - Progressively gets longer until QRS complex is DROPPED.

Heart Rate: Varies. Ventricle rate is less than the Atrial rate because some QRS complexes are dropped.
Atrial Rhythm: Regular
Ventricular Rhythm: IRRegular
P wave: Normal, consistent appearance, equal distance apart. More P waves than QRS complexes.

QRS complex: Some DROPPED. When present, normal duration < 0.12 secs

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72
Q

2nd deg Heart Block (AV Blocks)
Type 2 - Mobitz II

Causes:
Associated with heart disease and drug toxicity
Often progressive and results in decreased CO
Treat with pacemaker

A

A 2nd deg type 2 AV block is usually permanent, and is treated with a pacemaker.
(A end deg type 2 AV Block causes a sudden failure of impulse conduction from the atria to the ventricles without a progressive increase in conduction time)

PR interval: Normal or prolonged, but consistent (unlike 2nd deg block type 1)

Heart Rate: Varies. Ventricle rate is less than the Atrial rate because some QRS complexes are dropped.

Atrial Rhythm: Regular
Ventricular Rhythm: IRRegular
P wave: Normal, consistent appearance, equal distance apart. More P waves than QRS complexes.

QRS complex: Some DROPPED. When present, normal or wide duration

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73
Q

3rd Degree Heart Block (AV Blocks) - Complete Block

Causes and Tx:
Associated with severe heart disease, some systemic diseases, certain drugs
Usually results in decreased CO, ischemia, HF, and shock
Can lead to syncope
Treat with pacemaker
Drugs to increase heart rate if needed while awaiting pacing

A

A 3rd degree AV block is treated with a pacemaker.
(A 3rd degree AV block causes a complete failure of all impulse conduction from the atria to the ventricles.)

P wave: More P waves than QRS waves. P waves are NOT associated with QRS complexes. (P waves appear normal and consistent appearance.)

PR interval: varies
QRS comples: Normal or wide duration

Heart Rate: Atrial rate is normal (60 - 100 BPM). Ventrcular rate is slow < 60 BPM.

Atrial Rhythm: Regular
Ventricular Rhythm: Regular

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74
Q

A patient has a diagnosis of acute myocardial infarction, and his cardiac rhythm is sinus bradycardia with 6 to 8 premature ventricular contractions (PVCs) per minute. The pattern that the nurse recognizes as the most characteristic of PVCs is:
a.an irregular rhythm.
b.an inverted T wave.
c.a wide, distorted QRS complex.
d.an increasingly long PR interval.

A

Answer: C
A wide, distorted QRS complex

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75
Q

ST segment depression/ elevation indication

A
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76
Q

PVC
(Premature Venricular Contractions)

A

Associated with stimulants, electrolyte imbalances, hypoxia, heart disease
Not harmful with normal heart but may reduce CO, lead to angina and HF in diseased heart
Assess hemodynamic status

Treatment
Correct cause
β-blockers, lidocaine, or amiodarone

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77
Q

PAC for later
Contraction starting from ectopic focus in atrium in location other than SA node
Travels across atria by abnormal pathway, creating distorted P wave
May be stopped, delayed, or conducted normally at the AV node

A

Causes
Emotional stress
Physical fatigue
Caffeine
Tobacco
Alcohol
Hypoxia
Electrolyte imbalances
Disease states

Manifestations
Palpitations
Heart “skips a beat”
Treatment
Monitor for more serious dysrhythmias
Withhold sources of stimulation
β-blockers

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78
Q

Adenosine for SVT
(SVT is super tachy. HR> 150 bpm)

Tx: Vasovagal - Adenosine - Cardiovert

SVT = 1st non-invasive
Non-invasive process:
1. Vagal maneuver
2. Blow down straw continuously
3. Carotid massage
4. Cooling down the neck area measures.
Adenosine has 5-10 sec half-life so rapid push required 1-2 seconds followed by saline flush.

*NOTE
Adenosine is not a piggyback medicine, and is not given over 10 mins. Injection site should be close to the heart. Typically in the AC area – inside the elbow.

A

Atropine for Bradycardia

*Atropine for symptomatic bradycardia

*Atropine is anticholinergic/ antisecretions
*increases heart rate, as blood supply to vital organs increase, makes the body dry.
*You can’t pee with atropine, and HR really high like on top of the PINE tree.
*Symptomatic bradycardia with key signs of low oxygen, pale skin, cyanosis

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79
Q

Vasopressors
Epinephrine (adrenaline) and norepinephrine (Levophed)- Constricting the blood vessels, increasing the BP
*Epi and norepi are given for severely low BP like septic shock. To increase the BP.

Dopamine and Dobutamine = 2D for deeper contractions. given for deeper contraction. For Heart Failure, and low CO

Vasopressin and Desmopressin increases BP (are artificially made ADH drugs that increases fluid in the body and decreases urination.)

A

Epi is given first during cardiac arrest to initiate heart contractions

Epi for cardiac arrest as seen in asystole, PEA.

Others:
-Epi is used for anaphylactic shock
-Phentolamine = used to treat extravasation caused by epi and dopamine.
-Clonindine - puts BP down.

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80
Q

PAD and PVD

A
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81
Q

PAD and PVD note

A
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82
Q

Stroke Volume
(Hemodynamic terms)

A

Volume of blood (in liters) ejected from the left ventricle with each heartbeat.

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83
Q

CO def
(Hemodynamic terms)

A

Volume of blood (in liters) ejected from the left ventricle each min. Normal range = 4-8 L/min

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84
Q

CO formula

A

HR * SV
(Heart Rate * Stroke Volume)

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85
Q

HR

A

Number of times the ventricles contract each min. Normal: 60 - 100 beats/min

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86
Q

Patient Teaching on cardiac catherization

pre procedure interventions:

A

pre procedure interventions:
* get informed consent
* assess for dye allergies and check kidney function
* hold metaformin
* may clip hair (or shave site?)
* clean with antiseptic
* NPO beforehand
* assess distal pulses and VS / mark pulse with a sharpie
* if needed use a doppler for locating pulses

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87
Q

Patient Teaching on cardiac catherization

Teaching:

A

Teaching:
* may feel a warm flushing sensation or urge to urinate
* heart palpitations as the dye is injected

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88
Q

Patient Teaching on cardiac catherization

post-procedure interventions:

A

post-procedure interventions:
* keep leg straight for 4-6 hours to prevent bleeding
* if closure device is used, in bed for 1-2 hours
* encourage fluids to flush out dye
* assess pulses and VS for any changes or bleeding

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89
Q

Cardiac Biomarkers Def

A

Serum Cardiac Biomarkers are proteins released into the blood from necrotic heart muscle after an MI.
* Troponin is most specific

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90
Q

Serum Cardiac Bio-Markers

A
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91
Q

Preload
(Hemodynamic terms)

A

Volume of blood in ventricles at the end of diastole.

(just prior to contraction). Determines the amount of stretch placed on myocardial fibers.

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92
Q

Afterload
(Hemodynamic terms)

A

Peripheral resistance the left ventricle must overcome to push the blood into the systemic circulation.

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93
Q

LVEF
(Left Ventricle Ejection Factor)

A

Percentage of blood leaving the left ventricle each time it contracts.

Normal: 55 - 70%

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94
Q

Prinzmetal’s Angina or Variant Angina

A

Related to coronary artery spasm, occurs at rest.
#1 drug : Diltaizem

Prinzmetal’s angina almost always occurs when a person is at rest, usually between midnight and early morning

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95
Q

Angina (Chest Pain) due to ischemic heart disease types

A

*Unstable Angina is also called MI. It can be STEMI or NSTEMI. Occurs at rest or exercise.

*Chronic Stable Angina occurs w/exercise, relieved by rest or nitroglycerin. (consistent pattern for >= 2 months)

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96
Q

Angina vs MI

A

Chest pain unrelieved by rest or nitroglycerin lasting > 30 mins is indicative of a MI.

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97
Q

Aneurysm basics: def, RF, s/s

A

Baloon-like buldge in the arterial wall. Weakening of the arterial wall may be due to congential disorder, trauma, infection, or disease, damages.

RF: male, white ethinicity, Increase age, atherosclerosis, HTN, HLP, smoking, Marfan Syndrome

s/s: May be asymptomatic and found during routine tests.

(Marfan syndrome is a genetic condition that affects the body’s connective tissue. Connective tissue holds all the body’s cells, organs and tissue together.Marfan syndrome most commonly affects the heart, eyes, blood vessels and skeleton.)

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98
Q

Doubling:
Aneurysm def and RF

A

Outpouching or dilation of arterial wall
*Common problems involving aorta
*Occur in men more often than in women and in whites more often than African Americans
*Incidence ↑ with age

RF: Age
Male gender
High BP
Coronary artery disease
Family history
High cholesterol
Lower extremity PAD
Carotid artery disease
Previous stroke
Tobacco use
Being overweight or obese

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99
Q

2 types of aneurysm

A
  1. True -
    Wall of artery forms aneurysm
    At least one vessel layer still intact
    Further subdivided
    1.1 Fusiform
    Circumferential, relatively uniform in shape
    1.2 Saccular
    Pouchlike with narrow neck connecting bulge to one side of arterial wall
  2. False
    Also called pseudoaneurysm
    *Not an aneurysm
    *Disruption of all layers of arterial wall
    *Results in bleeding contained by surrounding structures
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100
Q

A. True fusiform abdominal aortic aneurysm. B. True saccular aortic aneurysm. C. False aneurysm or pseudoaneurysm. D., Aortic dissection.

A
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101
Q

Case Study:
E.O., a 74-year-old woman, comes to the ED with deep chest pain radiating throughout the chest to the back.
She reports that she smoked 1 pack of cigarettes/day for 20 years, quitting 5 years ago.
She weighs 212 lb.

A

Thoracic Aortic Aneurysm

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102
Q

Aneurysm basics: Nursing Care

A

Nursing Care:
Monitor for aortic rupture (sx: sudden onset of severe pain, s/s of hypovolemic shock, hypotension, diaphoresis, decrease LOC, oliguria, decrease pulses distal to rupture)

Montior VS, cardiac rhythm, ABGs, urine o/p.
Report output < 30 mL/hr

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103
Q

Aneurysm Causes

A

Causes:
Degenerative
Congenital
Mechanical
Penetrating or blunt trauma
Inflammatory
Infectious

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104
Q

Aneurysm basics: Dx and Tx

A

Dx: CT/ Ultrasound

Tx: *Prevention of aneurysm *medications - antiHTN
*surgery - aneurysm resection or repair.

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105
Q

Decrease Cardiac Output signs

A

Hypotension, pulmonary edema, decreased cerebral blood flow, cardiopulmonary arrest

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106
Q

AAA mimics

A

May mimic pain associated with abdominal or back disorders
May cause back pain, epigastric discomfort, altered bowel elimination, intermittent claudication
May spontaneously embolize plaque
Causing “blue toe syndrome”

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107
Q

Aortic Aneurysm Complication

A

Rupture
- Hemorrhage
- Cardiac Tampnade

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108
Q

Cardiac Tamponade (blood in pericardium sac) s/s or manifestations

A

Hypotension
Narrowed pulse pressure
Distended neck veins
Muffled heart sounds
Pulsus paradoxus

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109
Q

Aortic Aneurysm Prevention

A

Prevent Rupture, Early detection and Treatment

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110
Q

Aortic Aneurysm Size

A

Small aneurysm (4- 5.4 cm)
Conservative therapy used
Risk factor modification
↓ blood pressure
Ultrasound, MRI, CT scan monitoring every 6 to 12 months

5.5 cm is threshold for repair
Intervention at >5 cm in women with AAA
Surgical intervention may occur earlier in
Patients with a genetic disorder
Rapidly expanding aneurysm
Symptomatic patients
High rupture risk

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111
Q

AAA repair

A

Open repair. For this surgery, your doctor makes a large incision in the abdomen to expose the aorta. Once he or she has opened the abdomen, a graft can be used to repair the aneurysm. Open repair remains the standard procedure for an abdominal aortic aneurysm repair.
Incising diseased segment of aorta
Removing intraluminal thrombus or plaque

Endovascular aneurysm repair (EVAR). This is a minimally invasive option. This means it is done without a large incision. Instead, the doctor makes a small incision in the groin. He or she will insert special instruments through a catheter in an artery in the groin and thread them up to the aneurysm. At the aneurysm, your doctor will place the stent and graft to support the aneurysm.

112
Q

Potentially lethal complication in emergency repair

A

Intraabdominal hypertension (IAH)

Associated with abdominal compartment syndrome (ACS)
Reduces blood flow to viscera
End-organ perfusion impaired

113
Q

IAH treatment

A

Open surgical compression
Percutaneous drainage
Percutaneous drainage combined with tPA infusion

114
Q

Post-op AAA repair

A

Neuro: LOC, GI : urinary o/p, CVP/PA pressure, daily weight, peripheral pulses check, infection, continuous ECG monitoring

115
Q

AAA repair post-op - Pt. Teaching

A

Encourage patient to express concerns
Instruct patient to gradually increase activities
No heavy lifting
Teach about signs and symptoms of complications
Infection
Neurovascular changes

116
Q

Abdominal AAA assessments

A

Caution# Abdominal Aortic Aneurysm: do not palpate due to risk for rupture.

AAA s/s: Flank/ back pain, pulsating abdominal mass with bruit.

117
Q

Thoracic Aneurysms

A

Severe back/chest pain, SOB, Dysphagia (difficulty swallowing), cough

Often asymptomatic
Most common manifestation
Deep diffuse chest pain
Pain may extend to interscapular area

118
Q

Indications of Aneurysm rupture

A

Diaphoresis
Pallor
Weakness
Tachycardia
Hypotension

Monitor for indications of rupture
Abdominal, back, groin, or periumbilical pain
Changes in level of consciousness
Pulsating abdominal mass

119
Q

Descending Aortic Dissection def

A

Not a type of aneurysm
Result of a false lumen through which blood flows

120
Q

Aortic dissection prevalence, RF

A

Affects men more often than women
Occurs most frequently in sixth and seventh decades of life

121
Q

Aortic dissection patho

A

Due to degeneration of the elastic fibers in the arterial wall
Chronic hypertension hastens the process
Tear in inner layer allows blood to “track” between inner and middle layer

122
Q

Aortic dissection intial goal

A

HR and BP control
↓ BP and myocardial contractility to diminish pulsatile forces within aorta
Pain management

Drug therapy
IV β-adrenergic blocker
Esmolol (Brevibloc)
Other antihypertensive agents
Calcium channel blockers
Nitroprusside
Angiotensin-converting enzyme inhibitors
Morphine

CVD risk factor modification
Close surveillance with CT or MRI

123
Q

Types of Aortic dissection

A

Depend on location of intimal tear and extent of dissection

  1. Acute Type A aortic dissection
    Abrupt onset of excruciating anterior chest pain
  2. Acute Type B aortic dissection
    More likely to report pain located in their back, abdomen, or legs

Standard to treat acute and chronic Type B aortic dissections ——–
Thoracic endovascular aortic repair TEVAR similar to EVAR

124
Q

Aortic dissection s/s

A

Pain characterized as
Sudden, severe pain in anterior part of chest, or intrascapular pain radiating down spine to abdomen or legs
Described as “sharp” and “worst ever”
May mimic that of MI

125
Q

Following an aortic aneurysm repair, the patient suddenly develops severe pain in the right lower extremity. The right pedal pulse is decreased and the right foot is cool and pale. Which complication should the nurse suspect?
Hypothermia
Wound infection
Bleeding from the graft site
Embolization or graft occlusion

A

Embolization or graft occlusion

126
Q

Aneurysm

A

https://quizlet.com/189203445/exam-2-practice-questions-flash-cards/

127
Q

A patient who has had a femoral-popliteal bypass graft to the right leg is being cared for on the surgical unit. Which actin by the LPN/LVN caring for the patient requires the RN to intervene?

A

The LPN/LVN has the patient sit in a bedside chair for 90 min

128
Q

The community health nurse is planning health promotion teaching targeted at preventing coronary artery disease (CAD). Which ethnic group would the nurse select as the highest priority for this intervention?

A

White male

129
Q

Which antilipemic medications should the nurse question for a patient with cirrhosis of the liver (select all that apply)?

A

Ezetimibe (SE Upper Respiratory Infection)
Atorvastatin

Ezetimibe inhibits cholesterol absorption in the intestine whereas statins inhibit cholesterol production primarily in the liver

130
Q

The nurse would assess a patient with complaints of chest pain for which clinical manifestations associated with a myocardial infarction (MI) (select all that apply)?

A

Ashen skin
Diaphoresis
Nausea and vomiting
S3 or S4 heart sounds

131
Q

When planning emergent care for a patient with a suspected MI, what should the nurse anticipate administrating?

A

ONAM
Oxygen, nitroglycerin, aspirin, and morphine

132
Q

The nurse is examining the ECG of a patient who has just been admitted with a suspected MI. Which ECG change is most indicative of prolonged or complete coronary occlusion?

A

Pathologic Q wave

133
Q

Which patients are susceptible to infective endocarditis?

A

Patients with preexisting heart disease
Patients with HIV
Patients that require hemodialysis

134
Q

When a patient has mitral regurgitation, which abnormal heart sound is detected?

A

Systolic murmur

135
Q

Which of the following medical conditions are considered acute coronary syndromes?

A

Unstable angina
Myocardial infarction

136
Q

Desirable levels of cholesterol are ______ mg/dL and LDL is _____ mg/dL

A

less than 200; less than 130

137
Q

In which way do statins work to reduce atherosclerotic disease progression?

A

Increases LDL receptors on liver cells

138
Q

CAD typically presents with which classic symptom?

A

Angina pectoris

139
Q

Mr. G is unable to walk a block or climb one flight of stairs without getting chest pain. His chest pain is relieved with rest and two nitroglycerin tablets. What type of angina pectoris does he have?

A

Stable

140
Q

Which type of chest pain is not related to physical activity and often occurs at night?

A

Prinzmetal’s or variant angina

141
Q

Changes in which ECG waves are sensitive electrographic indicators of ischemia and injury to the myocardium?

A

ST segment

142
Q

A CK-MB level greater than _______ is indicative or cardiac muscle damage?

A

6%

143
Q

T wave inversion and ST segment depression are hallmarks of which condition?

A

MI

144
Q

For which reason may an exercise stress test be ordered?

A

To evaluate the patient’s likelihood of having altered myocardial tissue perfusion

145
Q

Patient’s with ECG changes suggestive of ischemia, but without the presence of serum biomarkers are diagnosed as having which coronary event?

A

Unstable angina

146
Q

Which ECG changes are indicative of an acute MI?

A

Hyperacute T wave
ST segment elevation
The presence of new left bundle branch block

147
Q

Therapies to inc myocardial perfusion include which goals?

A

Reducing the area of infarction
Increasing the likelihood that LV function will be preserved
Decreasing the likelihood of developing Q waves on ECG

148
Q

Which assessment finding may indicate that reocclusion has occurred after thrombolytic therapy?

A

Chest pain

149
Q

Which assessment is frequently obtained after PCI?

A

Palpation of pedal pulses

150
Q

The patient comes to the ED with severe, prolonged angina that is not immediately reversible. The nurse knows that if the patient once had angina related to a stable atherosclerotic plaque and the plaque ruptures, there may be occlusion of a coronary vessel and this type of pain. How will the nurse document this situation related to pathophysiology, presentation, diagnosis, prognosis, and interventions for this disorder?

A

Acute coronary syndrome (ACS)

151
Q

Postoperative care of a patient undergoing coronary artery bypass graft (CABG) surgery includes monitoring for what common complication?

A

Atrial dysrhythmias

152
Q

A patient was admitted to the emergency department (ED) 24 hours earlier with complaints of chest pain that were subsequently attributed to ST-segment-elevation myocardial infarction (STEMI). What complication of MI should the nurse anticipate?

A

Cardiac dysrhythmias

153
Q

The community health nurse is planning health promotion teaching targeted at preventing coronary artery disease (CAD). Which ethnic group would the nurse select as the highest priority for this intervention?

A

White male

154
Q

Intensive monitoring of the patient following an aortic aneurysm repair is required by the nurse because many body systems can be affected by:

A

ischemia from dislodged thrombi

155
Q

Which patient is at highest risk for hypoxemic respiratory failure?

A

A patient who has a massive pulmonary embolism

156
Q

A patient with severe chronic lung disease is hospitalized with respiratory distress. Which finding would suggest to the nurse that the patient has developed rapid decompensation?

A

Agitation or confusion

157
Q

When assessing a patient with sepsis, which finding would alert the nurse to the onset of acute respiratory distress syndrome (ARDS)?

A

Fine, scattered crackles on auscultation of the chest

158
Q

HF PPT#34

Heart Failure Risk Factors
HF can be caused by COPD, years of smoking. Or obstructive sleep apn

https://quizlet.com/83451982/cardiovascular-disease-flash-cards/
(referred for following cards)

A

Primary risk factors
Hypertension
Modifiable risk factor
CAD
Co-morbidities contribute to development of HF

159
Q

Heart block or MI = 3 most deadliest complications

A

 Sever low BP = cardiogenic shock
 VFib/ V Tach (Dysrhythmias)
 Heart Failure Heavy Fluid.

160
Q

Two complications of MI are pericarditis and mitral valve prolapse.

A

Inflammation of the sack around the heart can lead to pericarditis = pericardial effusions or cardiac tamponade. This is where the heart is switched to death with its own blood sac, causing the heart to stop beating.
With cardiac tamponade we always monitor for BEC = Big JVD, Extreme Low BP, Can’t hear the heart sounds, also called muffled or distal heart sounds.

161
Q

HF note

A
162
Q

Indicators of performing stress test

A
  • patient with symptoms of CAD
  • determination of pt. physical work capacity
  • determination of pt. functional capacity after MI
  • Evaluation of exercise-induced dysrhythmias
  • Evaluation of symptom-free pt. <40 at risks for CAD
  • Evaluation for dysrhythmias, angina, and ischemia
163
Q

The nurse would assess a patient with complaints of chest pain for which of the following clinical manifestations associated with a myocardial infarction (MI) (Select all that apply)?
A. Flushing
B. Ashen skin (pale)
C. Diaphoresis
D. Nausea and vomiting
E. S3 or S4 heart sounds

A

B, C, D, E

164
Q

When planning emergent care for a patient with a suspected MI, the nurse will anticipate administration of
A. Oxygen, nitroglycerin, aspirin, and morphine.
B. Oxygen, furosemide (Lasix), nitroglycerin, and meperidine.
C. Aspirin, nitroprusside (Nipride), dopamine (Intropin), and oxygen.
D. Nitroglycerin, lorazepam (Ativan), oxygen, and warfarin (Coumadin).

A

A

165
Q

Percutaneous Transluminal Coronary Angioplasty (PTCA)

A

Insertion of a wire sheath into the occluded or narrowed coronary artery
- Pt. will take Plavix after stenting

166
Q

Complications Of MI include

A
  • Dysrhythmias
  • Heart failure
  • Cardiogenic shock
  • Pericarditis
  • Dressler syndrome: pericarditis with effusion and fever that develops 4 to 6 weeks after MI. May be caused by an antigen-antibody response to necrotic myocardium
167
Q

A patient was admitted to the emergency department 24 hours earlier with complaints of chest pain that were subsequently attributed to ST-segment-elevation myocardial infarction (STEMI). Which of the following complications of MI should the nurse anticipate?

A. Unstable angina
B. Cardiac tamponade
C. Sudden cardiac death
D. Cardiac dysrhythmias

A

D

168
Q

For which of the following is percutaneous transluminal coronary angioplasty (PTCA) most clearly indicated?

A. Chronic stable angina
B. Left-sided heart failure
C. Coronary artery disease
D. Acute myocardial infarction

A

D

169
Q

Diagnosis for Patient with ACS

A
  • Ineffective cardiac tissue perfusion
  • Risk for fluid imbalance
  • Risk for ineffective peripheral tissue perfusion
  • Death anxiety
  • Deficient knowledge
170
Q

Goals of Nursing Care for Patient with Acute MI

A
  • Relief of pain or ischemic signs and symptoms,
  • prevention of further myocardial damage,
  • absence of respiratory dysfunction,
171
Q

percutaneous coronary intervention

A

invasive but nonsurgical intervention technique that is performed within 90 minutes of an acute MI diagnosis to bridge pt. to coronary bypass graft (CABG)

172
Q

cardiopulmonary bypass

A

used to provide oxygenation, circulation, and hypothermia during induced cardiac arrest

173
Q

nursing main assessments for postoperative period for CAGB is

A
  • fluid and electrolytes balance
  • hypothermia
  • hypertension
  • hypotension
174
Q

Myocardial Infarction is _________ and is due to ____ and can lead to _____

A

irreversible;
cell death;
scarring

175
Q

s/s of ACS

A
  • Chest Pain
  • Palpitations
  • Dyspnea
  • Cough
  • Wheezing
  • Anorexia
  • Nausea*
  • Vomiting*
176
Q

Chest Pain locations

A
  • upper chest
  • substernal radiating to neck and jaw
  • epigastric
  • substernal radiating down left arm
  • epigastric radiating from neck, jaw and arm
  • neck and jaw
  • left shoulder down both arms
  • intrascapular
177
Q

Angina Pectoris

A

A syndrome characterized by episodes of pain or pressure in the anterior chest caused by insufficient coronary blood flow due to emotional stress or physical exertion

178
Q

Stable angina

A

predictable and consistent pain that occurs on exertion - relieved by rest and/or nitroglycerin*

179
Q

Unstable angina (preinfarction angina or crescendo angina):

A

Symptoms increase in frequency and severity
- may not be relieved with rest or nitroglycerin (more severe)
- requires medical intervention!

180
Q

Variant angina

A
  • (Prinzmetal’s angina)
  • pain at rest with reversible ST- segment elevation
  • thought to be caused by coronary artery vasospasm
181
Q

Treatment of Angina

A
  • Elevate head of bed
    Morphine (for pain, vasodilator–> increase blood supply & CO)***
    Oxygen
    Nitrate (vasodilator= decreased oxygen demand)
    Aspirin (antiplatelet)
  • β-Adrenergic blockers: decrease myocardial oxygen demand by reducing HR, BP, and contractility
  • ACE inhibitors
  • cholesterol-lowering drugs
  • Stool softeners (avoid vavlsa manuveur)
182
Q

main nursing diagnose for Patient with Angina Pectoris

A

Ineffective cardiac tissue perfusion

183
Q

If pt. needs assistance for bathroom and has ECG elevation, nurse should

A

give bedpan (pt. should not ambulation, will need more oxygen supply)

184
Q

Clinical Manifestations of ACS Myocardial Infarction (MI)

A
  • Results from sustained ischemia
  • chest pain that last>20 minutes (causing irreversible myocardial cell death (necrosis)
  • Necrosis of entire thickness of myocardium takes 4 to 6 hours
  • decrease CO
  • decrease BP (systolic between 60-80)
185
Q

Cardiac Marker called Myoglobin is Released in __________ and increase levels within

A

skeletal or cardiac injury;
1 to 3 hours and peaks within 12 hours after the onset of symptoms

186
Q

Creatine Kinase found in cardiac muscle is called

A

MBCK-MB

187
Q

CK-MB increases levels within

A

4 to 8 hour window post injury
- within 12 to 24 hours this level elevates to approximately 5 to 15 times normal

188
Q

Troponin

For MI — If troponin is negative, we do the stress test. Here we stress out the heart with low oxygen.

A
  • Protein that helps regulate heart muscle contraction
  • Gold standard of care.
  • Remains elevated for 5-14 days.
  • Do not appear immediately in the serum, takes about 30 minutes
189
Q

after _____ days after MI, pt. can increase level of activity

A

10 to 14

190
Q

tPA
Fibrinolytic Administration for acute MI treatment

A

should be activated within 3 hours of ischemic stroke
- dissolves the fibrin binding the platelets together (tPA)

Goal of administration of a fibrinolytic is within 30 minutes of the arrival in the ED

191
Q

Which patient is most at risk for developing coronary artery disease?

A. A hypertensive patient who smokes cigarettes
B. An overweight patient who uses smokeless tobacco
C. A patient who has diabetes and uses methamphetamines
D. A sedentary patient who has elevated homocysteine levels

A

A

192
Q

CAD diagram

A

Partial occlusion of coronary artery: UA or NSTEMI
Total occlusion of coronary artery: STEMI

193
Q

CAD: manifestations of chronic stable angina

A

intermittent chest pain over a long period with the same patern of onset, duration and intensity of symptoms.
ST segment depression and or T wave inversion.
control with drugs.

194
Q

Diagram ACS

A
195
Q

Diagram STEMI and NSTEMI

A
196
Q

Clinical Manifestations MI - 1

A
197
Q

Clinical Manifestations MI -2

A
198
Q

Clinical Manifestations MI -3

A
199
Q

Clinical Manifestations MI - 4

A
200
Q

Complication of MI

A

Heart Failure

Heart failure - Occurs when pumping power of heart has diminished
Left-sided HF
Mild dyspnea, restlessness, agitation, slight tachycardia initially

Right-sided HF
Jugular venous distention, hepatic congestion, lower extremity edema

201
Q

Cardiogenic Shock

A

Cardiogenic shock
Occurs because of
Severe LV failure, papillary muscle rupture, ventricular septal rupture, LV free wall rupture, right ventricular infarction
Requires aggressive management
Associated with a high death rate

202
Q

Other complications of MI

A

Mitral valve regurgitation
Left ventricle aneurysm -
Myocardial wall becomes thinned and bulges out during contraction
Leads to HF, dysrhythmias, and angina

203
Q

Complication of MI - Acute Pericarditis

A

Pericarditis s/s
Mild to sever chest pain
Increases with inspiration, coughing, movement of upper body
Relieved by sitting in forward position
Pericardial friction rub
ECG changes

204
Q

MI complication - Dressler syndrome

A

Pericarditis and fever that develops 1 to 8 weeks after MI

Chest pain, fever, malaise, pericardial friction rub, arthralgia

High dose aspirin is treatment of choice

205
Q

Unstable Angina

A

Coronary angiography
For patients with a STEMI
Not for patients with UA or NSTEMI

Pharmacologic stress testing
For patients with abnormal but nondiagnostic ECG and negative biomarkers

206
Q

ACS treatment and nursing interventions steps

A

Initial interventions
12-lead ECG
Upright position
Oxygen – keep O2 sat > 93%
IV access
Nitroglycerin (SL) and ASA (chewable)
Statin
Morphine

Ongoing monitoring
Treat dysrhythmias
Frequent vital sign monitoring
Bed rest/limited activity for 12–24 hours
UA or NSTEMI
Dual antiplatelet therapy and heparin
Cardiac catheterization with PCI once stable

207
Q

NSTEMI

A

Reperfusion therapy

208
Q

Emergent PCI

A

Treatment of choice for confirmed STEMI
Goal: 90 minutes from door to catheter laboratory
Balloon angioplasty + stent(s)
Many advantages over CABG

209
Q

EXAM: Thrombolytic Therapy for STEMI - part -1

A

Thrombolytic therapy
Only for patients with a STEMI
Agencies that do not have cardiac catheterization resources

Given IV within 30 minutes of arrival to the ED

Patient selection critical

210
Q

EXAM: Thrombolytic Therapy for STEMI - part -2

A
211
Q

CABG surgery
Requires sternotomy and cardiopulmonary bypass (CPB)

Uses arteries and veins for grafts

The internal mammary artery (IMA) is most common artery used for bypass graft

A
212
Q

Radial Artery Graft

A
213
Q

Exam: Radial Artery Graft Assessment
Which assessment finding in a patient who has had coronary artery bypass grafting using a right radial artery graft is most important for the nurse to communicate to the health care provider?
a. Complaints of incisional chest pain
b. Pallor and weakness of the right hand
c. Fine crackles heard at both lung bases
d. Redness on both sides of the sternal incision

A

B

214
Q

When admitting a patient with a non-ST-segment-elevation myocardial infarction (NSTEMI) to the intensive care unit, which action should the nurse perform first?
a. Attach the heart monitor.
b. Obtain the blood pressure.
c. Assess the peripheral pulses.
d. Auscultate the breath sounds.

A

A

215
Q

Which information about a patient receiving thrombolytic therapy for an acute myocardial infarction is most important for the nurse to communicate to the health care provider?
a. An increase in troponin levels from baseline
b. A large bruise at the patient’s IV insertion site
c. No change in the patient’s reported level of chest pain
d. A decrease in ST-segment elevation on the electrocardiogram

A

C

(Continued chest pain suggests that the thrombolytic therapy is not effective and that other interventions such as percutaneous coronary intervention may be needed.

Bruising is a possible side effect of thrombolytic therapy, but it is not an indication that therapy should be discontinued.

The decrease of the ST-segment elevation indicates that thrombolysis is occurring, and perfusion is returning to the injured myocardium.

An increase in troponin levels is expected with reperfusion and is related to the washout of cardiac biomarkers into the circulation as the blocked vessel is opened.)

216
Q

The nurse obtains the following data when assessing a patient who experienced an ST-segment-elevation myocardial infarction (STEMI) 2 days previously. Which information is most important to report to the health care provider?
a. The troponin level is elevated.
b. The patient denies having a heart attack.
c. Bilateral crackles in the mid-lower lobes.
d. Occasional premature atrial contractions (PACs).

A

c
The crackles indicate that the patient may be developing heart failure, a possible complication of myocardial infarction (MI).

217
Q

A patient had a non-ST-segment-elevation myocardial infarction (NSTEMI) 3 days ago. Which nursing intervention is appropriate for the registered nurse (RN) to delegate to an experienced licensed practical/vocational nurse (LPN/VN)?
a. Reinforcement of teaching about the prescribed medications
b. Evaluation of the patient’s response to walking in the hallway
c. Completion of the referral form for a home health nurse follow-up
d. Education of the patient about the pathophysiology of heart disease

A

a
(LPN/VN education and scope of practice include reinforcing education that has previously been done by the RN.

Evaluating the patient’s response to exercise after a NSTEMI requires more education and should be done by the RN.

Teaching and discharge planning and referral are skills that require RN education and scope of practice.)

218
Q

After receiving a change-of-shift report about the following four patients on the cardiac care unit, which patient should the nurse assess first?
a. A 39-year-old patient with pericarditis who is complaining of sharp, stabbing chest
pain.
b. A 56-year-old patient with variant angina who is scheduled to receive nifedipine
(Procardia).
c. A 65-year-old patient who had a myocardial infarction (MI) 4 days ago and is
anxious about today’s planned discharge.
d. A 59-year-old patient with unstable angina who has just returned after a
percutaneous coronary intervention (PCI).

A

d
(After percutaneous coronary intervention (PCI), the patient is at risk for hemorrhage from the arterial access site.

The nurse should assess the patient’s blood pressure, pulses, and the access site immediately.

The other patients should also be assessed as quickly as possible, but assessment of this patient has the highest priority.)

219
Q

Which patient at the cardiovascular clinic requires the most immediate action by the nurse?
a. Patient with type 2 diabetes whose current blood glucose level is 145 mg/dL.
b. Patient with stable angina whose chest pain has recently increased in frequency.
c. Patient with familial hypercholesterolemia and a total cholesterol of 465 mg/dL.
d. Patient with chronic hypertension whose blood pressure today is 172/98 mm Hg.

A

B

220
Q

Which information collected by the nurse who is admitting a patient with chest pain suggests that the pain is caused by an acute myocardial infarction (AMI)?
a.
The pain increases with deep breathing.
b.
The pain has persisted longer than 30 minutes.
c.
The pain worsens when the patient raises the arms.
d.
The pain is relieved after the patient takes nitroglycerin.

A

B

221
Q

Which information given by a patient admitted with chronic stable angina will help the nurse confirm this diagnosis?
a.
The patient rates the pain at a level 3 to 5 (0 to 10 scale).
b.
The patient states that the pain wakes me up at night.
c.
The patient says that the frequency of the pain has increased over the last few weeks.
d.
The patient states that the pain is resolved after taking one sublingual nitroglycerin tablet.

A

D

222
Q

After the nurse has finished teaching a patient about use of sublingual nitroglycerin (Nitrostat), which patient statement indicates that the teaching has been effective?
a.
I can expect indigestion as a side effect of nitroglycerin.
b.
I can only take the nitroglycerin if I start to have chest pain.
c.
I will call an ambulance if I still have pain 5 minutes after taking the nitroglycerin.
d.
I will help slow down the progress of the plaque formation by taking nitroglycerin.

A

C

223
Q

After the nurse teaches the patient about the use of atenolol (Tenormin) in preventing anginal episodes, which statement by a patient indicates that the teaching has been effective?
a.
It is important not to suddenly stop taking the atenolol.
b.
Atenolol will increase the strength of my heart muscle.
c.
I can expect to feel short of breath when taking atenolol.
d.
Atenolol will improve the blood flow to my coronary arteries.

A

A

224
Q

The nurse will suspect that the patient with stable angina is experiencing a side effect of the prescribed metoprolol (Lopressor) if
a.
the patient is restless and agitated.
b.
the blood pressure is 190/110 mm Hg.
c.
the patient complains about feeling anxious.
d.
the cardiac monitor shows a heart rate of 45.

A

D

225
Q

Nadolol (Corgard) is prescribed for a patient with angina. To determine whether the drug is effective, the nurse will monitor for
a.
decreased blood pressure and apical pulse rate.
b.
fewer complaints of having cold hands and feet.
c.
improvement in the quality of the peripheral pulses.
d.
the ability to do daily activities without chest discomfort.

A

D

226
Q

A patient with a nonST-segment-elevation myocardial infarction (NSTEMI) is receiving heparin. What is the purpose of the heparin?
a.
Platelet aggregation is enhanced by IV heparin infusion.
b.
Heparin will dissolve the clot that is blocking blood flow to the heart.
c.
Coronary artery plaque size and adherence are decreased with heparin.
d.
Heparin will prevent the development of new clots in the coronary arteries.

A

D

227
Q

When administering IV nitroglycerin (Tridil) to a patient with a myocardial infarction (MI), which action will the nurse take to evaluate the effectiveness of the medication?
a.
Check blood pressure.
b.
Monitor apical pulse rate.
c.
Monitor for dysrhythmias.
d.
Ask about chest discomfort.

A

D

228
Q

A patient with ST segment elevation in several electrocardiographic (ECG) leads is admitted to the emergency department (ED) and diagnosed as having an ST-segment-elevation myocardial infarction (STEMI). Which question should the nurse ask to determine whether the patient is a candidate for fibrinolytic therapy?
a.
Do you take aspirin on a daily basis?
b.
What time did your chest pain begin?
c.
Is there any family history of heart disease?
d.
Can you describe the quality of your chest pain?

A

B

229
Q

Following an acute myocardial infarction (AMI), a patient ambulates in the hospital hallway. When the nurse is evaluating the patients response, which of these assessment data would indicate that the exercise level should be decreased?
a.
BP changes from 118/60 to 126/68 mm Hg.
b.
Oxygen saturation drops from 100% to 98%.
c.
Heart rate increases from 66 to 90 beats/minute.
d.
Respiratory rate goes from 14 to 22 breaths/minute.

A

C

230
Q

During the administration of the fibrinolytic agent to a patient with an acute myocardial infarction (AMI), the nurse should stop the drug infusion if the patient experiences
a.
bleeding from the gums.
b.
surface bleeding from the IV site.
c.
a decrease in level of consciousness.
d.
a nonsustained episode of ventricular tachycardia.

A

C

231
Q

**Three days after a myocardial infarction (MI), the patient develops chest pain that increases when taking a deep breath and is relieved by leaning forward. Which action should the nurse take next?
a.
Palpate the radial pulses bilaterally.
b.
Assess the feet for peripheral edema.
c.
Auscultate for a pericardial friction rub.
d.
Check the cardiac monitor for dysrhythmias.

A

C

232
Q

After the nurse teaches a patient with chronic stable angina about how to use the prescribed short-acting and long-acting nitrates, which statement by the patient indicates that the teaching has been effective?
a.
I will put on the nitroglycerin patch as soon as I develop any chest pain.
b.
I will check the pulse rate in my wrist just before I take any nitroglycerin.
c.
I will be sure to remove the nitroglycerin patch before using any sublingual nitroglycerin.
d.
I will stop what I am doing and sit down before I put the nitroglycerin under my tongue.

A

D

233
Q

When caring for a patient who has survived a sudden cardiac death (SCD) event and has no evidence of an acute myocardial infarction (AMI), the nurse will anticipate teaching the patient
a.
that sudden cardiac death events rarely reoccur.
b.
about the purpose of outpatient Holter monitoring.
c.
how to self-administer low-molecular-weight heparin.
d.
to limit activities after discharge to prevent future events.

A

B

234
Q

A patient admitted to the coronary care unit (CCU) with an ST-segment-elevation myocardial infarction (STEMI) is restless and anxious. The blood pressure is 86/40 and heart rate is 110. Based on this information, which nursing diagnosis is a priority for the patient?
a.
Acute pain related to myocardial ischemia
b.
Anxiety related to perceived threat of death
c.
Decreased cardiac output related to cardiogenic shock
d.
Activity intolerance related to decreased cardiac output

A

C

235
Q

When caring for a patient with acute coronary syndrome who has returned to the coronary care unit after having balloon angioplasty, the nurse obtains the following assessment data. Which data indicate the need for immediate intervention by the nurse?
a.
Pedal pulses 1+
b.
Heart rate 100 beats/min
c.
Blood pressure 104/56 mm Hg
d.
Chest pain level 8 on a 10-point scale

A

D

236
Q

A patient who has recently started taking rosuvastatin (Crestor) and niacin (Nicobid) reports all the following symptoms to the nurse. Which is most important to communicate to the health care provider?
a.
Generalized muscle aches and pains
b.
Skin flushing after taking the medications
c.
Dizziness when changing positions quickly
d.
Nausea when taking the drugs before eating

A

A

Severe muscle pain -This intense pain may be a symptom of rhabdomyolysis (rab-doe-my-OL-ih-sis), a rare condition that causes muscle cells to break down

237
Q

Colesevelam HLP drug

A

Take other meds after 2-4 hours of taking colesevelam.

238
Q

While awaiting diagnostic testing for MP what drug would you expect the health care provider to prescribe for MP to use if he develops the “indigestion” pain the next time he mows the lawn?

A

sublingual nitroglycerin

239
Q

CAD: medication Chronic stable angina

A

Goal is to decrease O2 demand and/or increase O2 supply.
1*line therapy: short-acting nitrates. dilate peripheral and coronary blood vessel –> SVR, venous pooling, decreased venous blood return to heart

240
Q

ACS: Complication of Myocardial Infarction

A

1*Dysrhythmias: Can be caused by ischemia, electrolyte imablances, or SNS stimulation. Life threatening dysrhythmias seen most often with anterior MI, heart failure, or shock.
Ventricular fibrillation, a common cause of sudden cardiac death (SCD) is a lethal dysrhythmia. it most often occurs within the first 4 hours after the onset of pain.

241
Q

Diagnosis to determine Unstable Angina or MI

A

include an1* ECG and serum cardiac marker.ECG: changes in QRS and ST segment, T wave.
patient with STEMI: tend to have a more extensive MI that is associated with prolonged and complete coronary occlusion, development of Q wave and ECG
Pts with NSTEMI: usually have transient thrombosis or incomplete coronary occlusion and usually do not develop patho Q wave

242
Q

MI: Serum Cardiac Markers

A

1* Troponin: CTnT and cTnI. increase 4-6 hrs peak 10 to 24 hrs and return 10 to 14 days. These markers are highly specific indicators of MI and have greater sensitivity.
CK-MB: 6 hrs peak 18 return 24 to 36. helps to know myocardial damage.
Myoglobin: 2 hrs peaks 3 to 15. lacks cardiac specificity.

243
Q

MI meds

A
  1. dobutamine
  2. dipyridamole
  3. adenosine
244
Q

ACS: Collaborative care what would you do? Initial intervention

A

12 lead ECG, semi-fowler’s position unless contraindicated and inititiate oxygen by nasal cannula to keep oxgygen saturation above 93, oxygen, IV access to provide an access for emergency, nitroglycerin and ASA, morphine sulfate for pain unrelieved by NTG.

245
Q

ACS: When PCI not available use thrombolytic therapy what is it?

A

Stops infarction process by dissolving thrombus, given by IV,

Inclusion criteria for thrombolytic therapy include (1) chest pain typical of acute MI 6 hours or less in duration, (2) 12-lead ECG findings consistent with acute MI, and (3) no absolute contraindications.

246
Q

ACS: Collaborative care what would you do for UA or NSTEMI medication

A

Ongoing monitoring: treat dysrhythmias, frquent vital sign monitoring, Bed rest/ limited activity for 12 - 24 hrs.
UA or NSTEMI med:
Aspirin, heparin and glycoprotein inhibitors (eptifibatide)
Coronary angiography with PCI once stable.

247
Q

A patient is admitted to the coronary care unit following a cardiac arrest and successful cardiopulmonary resuscitation. When reviewing the health care provider’s admission orders, which order should the nurse question?
a. oxygen at 4 L/ min per nasal cannhula
b. morphine sulfate 2 mg IV every 10 min until the pain is relieved
c. tissue plasminogen activator (t-PA) 100 mg IV infused over 3 hours
d. IV nitroglycerin at 5 mcg/minute and increase 5 mcg/minute every 3 to 5 min.

A

c. traumatic or prolonged cardiopulmonary resuscit ation is a relative contraindication for the administration of fibrinolytic therapy

248
Q

CAD meds

A

Lipid lowering
*statin - decrease production ny liver
*Ezetimibe (Zetia) - decrease lipid absoprtion by intestine.
*Bile acid sequestrants
Increase conversion of cholesterol to bile acids
Antiplatelet Therapy
ASA
Clopidogrel (Plavix)

249
Q

CAD meds

A

Lipid lowering
*statin - decrease production ny liver
*Ezetimibe (Zetia) - decrease lipid absoprtion by intestine.
*Bile acid sequestrants
Increase conversion of cholesterol to bile acids
Antiplatelet Therapy
ASA
Clopidogrel (Plavix)

250
Q

Revision Chronic Stable Angina clinical manifestations

A
251
Q

Slient Ischemia (a type of chronic stable angina)

A

Associated with diabetes neuropathy

252
Q

Chronic Stable Angina meds

A

ACE, ARBs, Beta blockers, CCB,
Lipid lowering drugs
Sodium current inhibitor
Ranolazine (Ranexa)

*Ranalazine treats chronic stable angina

253
Q

What is pulsus alternans on ECG?

A

CHF

Pulsus alternans is a physical finding with arterial pulse waveform showing alternating strong and weak beats. It is almost always indicative of left ventricular systolic impairment, and carries a poor prognosis

254
Q

Pulses Paradoxus

A

Seen in cardiac tamponade, chronic sleep apnea, croup, and obstructive lung disease (e.g. asthma, COPD).

Cause; pericardial effusions

Def: exaggerated drop in systemic blood pressure during inspiration is termed pulsus paradoxus

255
Q

Objective data for ACS

A
256
Q

Acute Intervention for Chronic Stable Angina

A
257
Q

Acute Coronary Syndrome = Coronary Revascularization

A
258
Q

Complications related to CardioPulmonary Bypass

A

Bleeding at insertion site
anemia from damage to RBCs and platelets
Hypovolemia
Monitor for afib (which is common)
Fluid and electrolyte imbalances
Hypothermia as blood is cooled as it passes through the bypass machine
Infections
Cognitive impairment
Pain Mgmt, DVT prevention, Pumonary hygiene

259
Q

Resumption of sexual activity post MI

A

Resumption of sexual activity
Teach when discuss other physical activity
Erectile dysfunction drugs contraindicated with nitrates
Prophylactic nitrates before sexual activity
When to avoid sex
Typically 7–10 days post MI or when patient can climb two flights of stairs

260
Q

Sudden Cardiac Death
Death within 1 hour of onset of acute symptoms

A

24-hour Holter monitoring
Exercise stress testing
Signal-averaged ECG
Electrophysiologic study (EPS)
Implantable cardioverter-defibrillator (ICD)
Antidysrhythmic drugs
LifeVest

261
Q

Acute Decompensated HF (ADHF)

A

Can manifest as pulmonary edema
Life-threatening situation – alveoli fill with fluid
Most commonly associated with left-sided HF

262
Q

Pulmonary Edema s/s

A

Pink -frothy sputum, pale+cyanoic+cool + clammy, tachycardia, dyspnea

263
Q

Chronic Heart Failure signs

A

Fatigue
Chest congestion/cough
Shortness of breath
Dyspnea
Orthopnea
Paroxysmal nocturnal dyspnea
Tachycardia
Edema
Limitation of Activities

264
Q

HF complications

A

Pleural effusion
Dysrhythmias – atrial and ventricular
Left ventricular thrombus
Hepatomegaly
Renal failure

265
Q

ADHF drugs

A

Diuretics
Decrease volume overload (preload)
Loop diuretics - Furosemide (Lasix)
Vasodilators
Reduce circulating blood volume and improve coronary artery circulation
IV nitroglycerin
Sodium nitroprusside
Nesiritide (Natrecor)

Morphine
Reduces preload and afterload
Relieves dyspnea and anxiety
Positive inotropes
β-agonists (dopamine, dobutamine, norepinephrine [Levophed])
Phosphodiesterase inhibitor (milrinone)
Digitalis

266
Q

Chronic HF drugs

A

RAAS inhibitors
ACE inhibitors
Angiotensin II receptor blockers
Aldosterone antagonists
Monitor potassium levels (hyperkalemia)

β-Blockers
Vasodilators
Nitrates
Combination therapy
BiDil
Positive inotropic agents
Digitalis

267
Q

Chronic HF - nutritional diet

A

Low sodium diet
Individualize recommendations and consider cultural background

Recommend Dietary Approaches to Stop Hypertension (DASH) diet
Sodium is usually restricted to 2 g/day

268
Q

Chronic HF nursing considerations

A

Fluid restriction not generally required
If required, < 2L/day
Ice chips, gum, hard candy, ice pops to help thirst
Daily weights important
Same time, same clothing each day
Weight gain of 3 lb (1.4 kg) over 2 days or a 3- to 5-lb (2.3 kg) gain over a week should be reported to HCP

269
Q

Chronic HF Nursing Diagnosis

A

Impaired gas exchange
Decreased cardiac output
Excess fluid volume
Activity intolerance

270
Q

Chronic HF - interventions

Successful eval:
Oxygen saturation, assessment of lung sounds, respiratory rate, capillary refill, assessment of peripheral edema, daily weights, intake and output, verbalizes understanding of teaching.

A

Monitor respiratory status
Administer oxygen therapy
Semi-Fowler’s position
Monitor hemodynamic status
Daily weights
I and O
Administer prescribed drugs
Monitor edema
Alternate rest with activity
Provide diversionary activities

Monitor response to activity
Collaborate with OT/PT
Reduce anxiety
Evaluate support system
Patient teaching

271
Q

A patient with a history of chronic heart failure is hospitalized with severe dyspnea and a dry, hacking cough. Assessment findings include pitting edema in both ankles, BP 170/100 mm Hg, pulse 92 beats/minute, and respirations 28 breaths/minute. Which explanation, if made by the nurse, is most accurate?
a. “The assessment indicates that venous return to the heart is impaired, causing a decrease in cardiac output.”
b.“The manifestations indicate impaired emptying of both the right and left ventricles, with decreased forward blood flow.”
c.“The myocardium is not receiving enough blood supply through the coronary arteries to meet its oxygen demand.”
d.“The patient’s right side of the heart is failing to pump enough blood to the lungs to provide systemic oxygenation.”

A

Answer: B
Rationale: The patient is experiencing acute decompensated heart failure with symptoms of both right- and left-sided heart failure. Left-sided heart failure prevents normal, forward blood flow and causes pulmonary congestion. Right-sided heart failure causes a backup of blood and results in venous congestion.

272
Q

A patient with left-sided heart failure is prescribed oxygen at 4 L/min per nasal cannula, furosemide (Lasix), spironolactone (Aldactone), and enalapril (Vasotec). Which assessment should the nurse complete to best evaluate the patient’s response to these drugs?
a.Observe skin turgor
b.Auscultate lung sounds
c.Measure blood pressure
d.Review intake and output

A

Answer: B
Rationale: Left-sided heart failure will prevent normal blood flow and will cause blood to back up into the left atrium and into the pulmonary veins. The increased pulmonary pressure causes fluid extravasation from the pulmonary capillary bed into the interstitium and then the alveoli, which manifests as pulmonary congestion and edema. The most important assessment to determine if the drugs are improving the patient’s condition is to auscultate lung sounds. The other assessments are important, but the best indicator of improvement of left ventricular function is a reduction in adventitious lung sounds (crackles).

273
Q

The home care nurse visits a patient with chronic heart failure who is taking digoxin (Lanoxin) and furosemide (Lasix). The patient complains of nausea and vomiting. Which action is most appropriate for the nurse to take?
a.Perform a dipstick urine test for protein.
b.Notify the health care provider immediately.
c.Have the patient eat foods high in potassium.
d.Ask the patient to record a weight every morning.

A

Answer: B
Rationale: Administration of furosemide increases excretion of potassium and may cause hypokalemia. The risk for digitalis toxicity increases if potassium levels are below normal and digoxin is administered. Signs and symptoms of digitalis toxicity include anorexia, nausea and vomiting, visual disturbances (such as “yellow” vision), and dysrhythmias.

274
Q

Exam: HF - Diagnostic test

A

*Echocardiogram
Provides information on *EF, heart valves and heart chambers
*ECG, chest x-ray, 6-minute walk test, MUGA scan, *cardiopulmonary exercise stress test, *cardiac catheterization, EMB
*BNP levels
Determine and treat underlying cause

275
Q

HEART BLOCK ULTIMATE GUIDE

A
276
Q

NCLEX: Bradycardia

A
277
Q

Raynaud vs Buerger

A

110_Cardiac (8 decks)

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