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NURSING 2 > Cardiac A&P CAD week 1 > Flashcards

Cardiac A&P CAD week 1 Flashcards

1
Q

Perfusion: Priority assessment

A 
BP 
MAP
Pulses 
Cap Refill 
LOC
Bowel Sounds
Urine Output 
Pain 
Skin Color 
Temperature
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2
Q

Perfusion: how do we know perfusion is adequate?

A 
A/O
MAP > 65 
UOP > 30 mL/hr
Pulses wnl
Warm to touch 
Tissue color wnl
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3
Q

What are priority labs for perfusion?

A 
Priority Labs
Hgb/Hct, 
RBC 
Protein/Albumin 
BUN/Creat 
Cardiac & Liver Enzymes 
BNP
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4
Q

What are signs of inadequate perfusion?

A 
Light headed Confused 
Sensation loss
Decreased organ function
Ischemic pain
Cell & Tissue necrosis
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5
Q

Describe the blood flow through the heart

A

Blood comes from periphery, RA, RV, pulmonary vasc., LA, LV, out thru aorta to rest of body

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6
Q

Preload

A

volume of blood in ventricles at end of diastole (end diastolic pressure)

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7
Q

What might preload be increased?

A

hypervolemia
regurgitation of valvse
HF

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8
Q

Afterload

A

Resistance left ventricle must overcome to circulate blood

the pressure the heart is pressing against

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9
Q

When might afterload be increased?

A

hypertension

vasoconstriction

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10
Q

What should a nurse do if patient has low CVP?

A

fluid replacement

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11
Q

What should a nurse do if patient is hypervolemic?

A

adminster diuretic

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12
Q

What should right atrial pressure be?

A

2-8 mmHg

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13
Q

What should systolic pulmonary pressure be?

A

15-25 mmHg

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14
Q

What should diastolic pulmonary pressure be?

A

8-15mmHg

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15
Q

What is the SA node?

A

Pace maker of heart; initiates heart beat for atrium

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16
Q

What is AV node?

A

AV node = gate keeper; decides how many beats get to go through to ventricle

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17
Q

What is s3 heart sound

A

Extra heart sound - indicates that patient has extra volume on boared; however, this can be normal in children and pregnant women

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18
Q

What is s4 heart sound

A

Abnormal, heart is resistant to volume coming in

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19
Q

Describe the 5 areas for listening to the heart and where they are?

A

a. Aortic: R 2nd intercostal space
2. Pulmonic = L 2nd intercostal space
3. Erb’s point = S1 and S2, L 3rd intercostal space
4. Tricuspid = Lower left sternal border, 4th intercostal
5. Mitral = L 5th intercostal, medial to midclavicular line

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20
Q

Geriatric considerations: mycocardium

A

Thicker and stiffer valves (calcified)
SNS does not respond as well
Baroreceptors do not respond as fast to pressure changes
Aorta and arteries calcify

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21
Q

Geratric considerations: women

A

Heart and it’s vessels are smaller; harder to work on; more effort

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22
Q

geriatric considerations:

A

Onset of heart disease sooner than females

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23
Q

CAD patho

A

Lipids deposit leading to endothelial injury and inflammation of the artery

    • progressive disease
    • fatty streaks
    • fibrous plaques
    • complicated lesions with thrombus formation
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24
Q

CAD assessment

A

family hx
non-modifiable risk factors
s/s occlusion (angina and poor perfusion)
risk factors / lifestyle

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25
Q

CAD labs and diagnostics

A
  • C Reactive Protein
  • Serum Cholesterol Levels
  • Fasting Glucose > 100 mg/dL increases the risk
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26
Q

What is C reactive protein

A

measures inflammation

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27
Q

CAD interventions

A

Promote PA and nutrition
Stop smoking, drinking too much and using substances
Monitor blood levels with risk assessment

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28
Q

CAD Complications

A

ACS / unstable angina
MI
Sudden cardiac event that can be fatal

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29
Q

CAD medications

A

Simvastatin and Niacin (for cholesterol)
Low dose aspirin
Ezetimbe (lowers cholesterol)

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30
Q

CAD education

A

diet decreased in saturated fat and increase in plan based - polyunsaturated

exercise 30 minutes a day most days

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31
Q

What to obtain from health hx

A 
family hx
hx s/s
common complications
medications
nutrition elimination
activity
sleeo
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32
Q

What do we evaluate with the lungs

A

Hemoptysis
Cough
Crackles
Wheezes

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33
Q

What do we evaluate with the abdomen

A 
Distension
Hepatojugular reflux
   - Patients reclining and as you push on liver 
Pulsatile mass
   - Anuerism in abd
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34
Q

What are common skin findings with CAD

A 
Clubbing
Cool skin & diaphoresis
Cold, pain or pallor of toes or fingertips
Peripheral cyanosis
Ecchymosis or bruising
Edema
Hematoma
Pallor
Rubor
Feet and ankle ulcer
Thinning of skin around a pacemaker or defibrillator
Xanthelasma (yellow plaques observed along nasal portion of eyelids)
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35
Q

Why would an angioplasty be used and how does it work?

A

USE: Build up of cholesterol partially blocking bloodflow through artery

a. stent with balloon inserted into partially blocked artery
b. balloon inflated to expand stent
c. balloon removed from expanded stent
d. the expanded stent now allows for adequate blood flow

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36
Q

Cardiac markers: Troponin

A

Should be less than 0.4

Peak in 10-12 hours, normalize in 10-14 days

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37
Q

Cardiac markets: Ck with MB

A

38-174 u/L

MB< 5% increase 4 hours peak 24 normal 48

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38
Q

Cardiac markers: myoglobin

A

(5-70 mcg/mL, increase 1-3 hour peak 12 hour)

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39
Q

What values should the 4 different types of lipids be at?

A

Cholesterol < 200
Triglycerides < 150
LDL 100-129
HDL 60

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40
Q

Brain naturetic peptide range

A

< 100

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41
Q

C reactive protein value

A

< 3.0

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42
Q

Homocysteine value

A

4-15

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43
Q

Holter monitor

A

ECG someone wears for couple of weeks to evaluate heart

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44
Q

Implantable loop recorders

A

only record when patient has s/s

used for infrequent s/s of patients

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45
Q

Trans telephonic monitoring

A

Transmit ECG via telephone

Diagnose arrhthmias and pacemaker evaluation

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46
Q

Wireless moblie cardiac monitoring systems

A

Transmits arrythmias via telephone for early intervention; can be challenging for elderly

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47
Q

What is an electrocardiogram?

A

Shows the electrical impulses thru the heart

- each phase of the cardiac cycle is reflected by specific wave forms

48
Q

What are the different waves of ecg and what do they represent?

A

P wave - atrial depolarization (atrial contraction)
QRS complex - ventricular depolarization (ventricle contraction)
T wave - ventricular repolarization (ventricle relaxing)
U wave - relaxing of purkinje fibers

49
Q

Where does atrial contraction (P wave) take place?

A

SA node

- atrium in heart contracting (depolarization)

50
Q

what is a U wave?

A

not common in clinical setting - believed to be produced by the resting of the purkinje fibers

51
Q

PR interval

A

starts at the P wave (atrial contraction), ends right before ventricle contraction

ends essential at the AV node (gatekeeper)

52
Q

ST segment

A

starts at end of QRS complex (ventricular contraction), and ends right before T wave

important when diagnosing MI

53
Q

What are arrhythmias / dysrhythmia?

A

disorder of the formation or conduction (or both) of the electrical impulse within the heart, altering the heart rate, heart rhythm, or both and potentially causing altered blood flow

54
Q

What people are at risk for arrhythmias?

A

Aging population, heart disease, polypharmacy, drug interactions with drug users

55
Q

What is a condition in which you would see a U wave

A

hypokalemia

56
Q

How are readings of ecg categorized

A

sinus
atrial
ventricular

57
Q

How do you tell the heart rate on ECG

A

count each QRS segment (1 segment = 1 heart beat)

58
Q

What is a sinus arrhythmia?

A

Sinus nose creates an impulse at an irregular rhythm; clinically insignificant

59
Q

When might we see sinus arrhythmia?

A

sometimes associated with respiratory cycle

occurs frequently in young and decreases frequently with age

60
Q

Describe sinus arrhythmias in comparison with respirations

A

Rate is the arrhythmia increases with inspiration and decreases with expiration

61
Q

What is sinus rhythm?

A

the normal rhythm of the heart where electrical stimuli are initiated in the SA node, and are then conducted through the AV node and bundle of His, bundle branches and Purkinje fibres. Depolarisation and repolarisation of the atria and ventricles show up as 3 distinct waves on ECG.

62
Q

Sinus bradycardia: patho

A

Sinus nose creates a slower than normal rate

63
Q

What may cause sinus bradycardia?

A 
lower metabolic needs 
vagal stimulation
medications
increased ICP
MI
64
Q

What are clinical manifestations of sinus bradycardia?

A

Rate less than 60 BPM; all other measurements on ECG are normal

Serious: confusion, chest pain, hypotension

65
Q

Sinus bradycardia: medical and nursing management

A

Only treated is serious s/s present
- confusion, chest pain, hypotension

hypotension –> trancutaneous pacing, atropine, dopamine or epinephrine (atropine first)

66
Q

Sinus tachycardia: patho

A

Sinus nose creases an impulse that is faster than normal

67
Q

Sinus tachycardia: cause

A

Physiologic (compensating for o2 demands), stress, medications that stimulate SNS

68
Q

Sinus tachycardia: clinical manifestations and assessment

A

Rate greater than 100 BPM

All other measures are normal

69
Q

Sinus tachycardia: medical and nursing management

A

ID and treat cause

Fluid replacement if patient is hypovolemic

70
Q

Atrial flutter: patho

A

atrium impulses at regular but rapid rate (between 220-350 times per minute)

SA node letting out many impulses and the ”gate keeper” (AV node) says no no no no no (stays closed)…OKAY you can go thru (opens) and this is all the fluttering you see on the ECG

71
Q

What do you see on ECG with atrial flutter

A

No P wave - flutter wave

72
Q

What might cause atrial flutter?

A

emboli

73
Q

Atrial flutter: clinical manifestations and assessment

A

may or may not be symptomatic

74
Q

Atrial flutter: clinical and nursing management

A

Cardioversion

Ablation

75
Q

Atrial flutter: medical management

A 
DIG
BB
Calcium channel blockers
Amiodarone
Anticoagulant
76
Q

Atrial fibrillation: patho

A

Atria is fibrillating – not even a controlled attempt at contraction
– think of wiggling a bowl of jello

20-30% of blood in that chamber going to ventricle – loss of volume

77
Q

Who is at risk for a fib

A

Age, valvular heart disease, CAD, hypertension, heart failure, cardiomyopathy, DM, OSA, obesity, pulmonary disease, hyperthyroidism, surgery (open heart)

5 time increase risk for CVA r/t emboli

78
Q

Atrial fibrillation: clinical manifestations and assessment

A

may or may not be symptomatic

decrease cardiac output r/t decrease filling time

79
Q

Atrial fibrillation: medical and nursing management

A

Control ventricular rate
Prevent thromboembolism
Cardioversion (rhythm control)

80
Q

Atrial fibrilation: medications

A 
Dig
BB
Ca2+ channel blockers
Amiodarone 
Anticoagulants
81
Q

Premature ventricular complex: patho

A

Starts in the ventricle and conducted before the next normal sinus impulse

82
Q

Premature ventricular complex: causes

A

Caffeine, nicotine, alcohol
acidosis, hypokalemia, hypoxia
increased occurance with aging and considered a marker in CHF

83
Q

What can premature ventricular complex lead to?

A

cardiac ischemia and infarction

84
Q

Premature ventricular complex: clinical manifestations and assessment

A

Bigeminy, trigeminy, couplet, triplet

Multifocal, unifocal

85
Q

Premature ventricular complex: medical and nursing management

A

treat cause (hypokalemia

86
Q

Ventricular tachycardia: patho

A

Three or more ventricular beats at a rate of 100bpm

87
Q

Ventricular tachycardia: causes

A

MI, hypokalemia hypomagnesemia, CMP, long QT

88
Q

Ventricular Tachycardia: clinical manifestations and assessment

A

Monomorphic or polymorphic (torsades)

Decreased cardiac output, pulselessness

89
Q

Ventricular Tachycardia: management

A

Amiodarone
Lidocaine
BB
Cardioversion or defibrillation

90
Q

Ventricular fibrillation: patho

A

Rapid, disorganized ventricular rhythm

Unsuccessful treatment of VT

91
Q

Ventricular fibrillation: manifestations

A

irregular
pulseless
cardiac arrest and death are imminent

92
Q

Ventricular fibrillation: management

A 
CPR
Defibrillation
Epinephrine 
Amiodarone
Lidocaine
Magnesium
93
Q

Ventricular asystole: patho

A

No cardiac activity

94
Q

Ventricular asystole: manifestations

A

no pulse, death is imminent

95
Q

Ventricular asystole: management

A

CPR
Poor prognosis
Hypothermia is really only good change for recovery

96
Q

What are signs and symptoms of low blood pressure?

A 
Dizzy/light headed
Blurred vision
Rapid HR
Fatigue
Lack of concentration
Cold, clammy skin
97
Q

Pulseless electrical rhythm: patho

A

may have organized electrical rhythm on the monitor but not breathing and pulseless

98
Q

Pulseless electrical rhythm: causes

A

Temperature, tamponade, toxins, hypovolemia, electrolytes (K+), acidosis

99
Q

Pulseless electrical rhythm: management

A

CPR

100
Q

Heart blocks

A

Occur when there is damage to the conduction system of the heart OR ischemia

101
Q

Heart block - new onset

A

new onset is a sign of worsening symptoms or can be precursor to further blocks rhythm changes

102
Q

What are the types of heart blocks

A

First degree AV block
Second degree type II
3rd degree
total

go look at the ECG of these slide 48

103
Q

What are the types of pacemaker therapy

A

transcutaneous
endocardial leads
transvenous
dual chambers

104
Q

What should you see on ECG when someone has a pacemaker

A

Pacemaker spike, ECG complex should follow
P wave should follow an atrial pacer
QRS should follow a ventricular pacer
- capturing

105
Q

Pacemaker therapy: complications

A 
bleeding
infection
displacement of leads
restrictions following placement
patient should know rate
106
Q

Electrical cardioversion

A

Delivery of a timed electrical current to terminate a tachyarrythmia

The defibrillator is set to synchronize and discharge during the ventricular depolarization

Synchronize prevents the delivery on the T wave, which could result in V fib

107
Q

What are nursing assessments for someone who is receiving cardioversion?

A

DIG held 48 hours prior
NPO at least 4 hours
Monitor airwar
Assess for signs of embolism

108
Q

What do electrical cardioversion joules depend on?

A

type of technology and arrhythmia: 50-200

109
Q

What is defibrillation?

A

Used on patient WITHOUT pulse - not used with patient has pulse
200-360 joules
not synchronized
CPR immidiately following defibrillation of there is not a return of pulse

110
Q

Implantable cardiac defibrillator: use

A

terminates life threatening episodes of tachycardia or fibrillation

111
Q

Deactivation of subcutaneous implantable cardioverter defibrillator (S-ICD) at end of life

A

will allow the natural death to occur instead of the shocks with arrhythmia at the end of life

112
Q

Cardiac arrest: patho

A

ventricular fibrillation OR ventricular tachy; profound bradycardia

    • asystole
    • PEA
113
Q

Cardiac arrest: manifestations

A

Consciousness BP pulse are lost, eyes begin dilating within 45 seconds, seizures may or may not occur

114
Q

Cardiac arrest: emergency management

A

CPR

CAB (Compression, airway, breathing)

115
Q

How long does a normal PR interval last

A

0.12-0.20 seconds

116
Q

how long is each small box on the EKG?

A

0.4 seconds

117
Q

What are the 5 steps to interpreting ECG?

A
  1. P waves presents? How many in 6 seconds
  2. P waves regular?
  3. R waves regular?
  4. How many R waves in 6 seconds
  5. Length or PR interval and length of QRS complex

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