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BEACON MedSurg/Peds > Test 3 Perfusion > Flashcards

Test 3 Perfusion Flashcards

1
Q

4 unique components of cardiac cells

A

conductivity, excitability, automaticity, contractility

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2
Q

the pathway of cardiac conduction

A

sinoatrial node–>internodal pathways–>atrioventricular node—>bundle of His–>Right bundle branch—>left bundle branch—> Purkinje fibers

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3
Q

60-100 beats per minute conduction origination

A

SA node

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4
Q

40-60 beats per minute conduction origination

A

AV node

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5
Q

Ventricle 20-40 beats per minute conduction origination

A

Ventricle

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6
Q

horizontal lines on the EKG paper measure

A

force of the electrical impulse is measured by amplitude (voltage)

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7
Q

verticle lines in EKG

A

measure time

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8
Q

.04 seconds on EKG=

A

small square

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9
Q

0.2 seconds on EKG strip =

A

heavy line, or 5 small squares

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10
Q

1 second on EKG strips =

A

5 large squares

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11
Q

1 minute =

A

3 hatch marks

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12
Q

P wave form represents

A

atrial depolarization (contractions) and emptying of the right and left atria

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13
Q

PR interval represents

A

the time it takes and electrical impulse to be conducted through the atria and the AV node, until the implulses cause ventricular filling and begins to cause ventricular depolarization (contraction)

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14
Q

QRS complex represents

A

ventricular depolarization, an electrical activity that causes both ventricles to contract and send blood out into the body

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15
Q

ST segment

A

portion of the line that leads from the end of the S wave to the beggining of the T wave, may be normal (flat), elevated, or depressed

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16
Q

T wave

A

follows ST segment, represents ventricular repolarization

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17
Q

1st step in EKG analysis

A
  • assess for P waves
  • Is there a P wave for every QRS
  • Are the P waves upright and the same shape
  • is the P-P interval (distance between consecutive P waves) regular
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18
Q

Step 2 in EKG analysis

A
  • Assess the P to QRS relationship
  • Is there a P wave before each QRS and a QRS after every P wave QRS complexes
  • Are they the same shape or do they vary
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19
Q

Step 3 EKG analysis

A
  • determine HR
  • if HR greater than 100: tachy
  • if HR lower than 60: brady
  • assess how the pt. is tolerating the rhythm
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20
Q

Step 4 EKG analysis

A
  • Determine regularity-is it regular, regular but interrupted, or irregular
  • compare r-r intervals
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21
Q

Step 5 EKG analysis

A
  • determine interval durations
  • what are the PR and QRS intervals
  • are the intervals within normal limits
  • are the intervals constant or do they vary
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22
Q

Step 6 EKG analysis

A
  • identify abnormalities and note the presence and frequency of ectopic or premature beats
  • is the ST segment flat, elevated (injury to heart muscle), depressed (ischemia, digitalis toxicity)
  • is the T wave rounded and upright or is it inverted (ischemia) or peaked (electrolyte with potassium or calcium out of balance)
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23
Q
  • rate is 60-100 BPM
  • rhythm: regular
  • P wave: one before each QRS
  • PR interval: 0.12-0.20 constant
  • QRS interval: <0.12
A

normal sinus rhythm

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24
Q

rate: <0.12

A

Sinus Bradycardia

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25
Q

in response to sinus brady interventions

A

carotid sinus massage, hypothermia, increased vagal tone, administration of parasympathomimetic drugs

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26
Q

hypothyroidism, increased intracranial pressure, obstructive jaundice, inferior wall MI
* all disease states causing which rhythm?

A

disease states with sinus brady

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27
Q

dizziness or syncope, weakness, pallor, diaphoresis, hypotension, angina, confusion, SOB
*all indicate

A

sinus brady

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28
Q

treatment of sinus brady

A

oxygen, atropine, pacemaker, additional medications

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29
Q

rate: 100-160, rhythm, p wave, pr and qrs interval are normal

A

sinus tachy

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30
Q

exercise, emotional stress, fever, pain, hypovolemia, anemia, myocardial ischemia, HG, thyrotoxicosis, EtOH/EtOH withdrawal
*all clinical associations with which rhythm

A

sinus tachy

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31
Q

hypotension, lightheadedness, palpitations, chest pain, restlessness, anxiety
*symptoms of

A

sinus tachy

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32
Q
  • oxygen
  • beta-adrenergic blockers
  • analgesics
  • antipyretics and antibiotics
  • diuretics and inotropic agents
  • fluid replacement
  • all treatments done for which rhythm
A

sinus tachy

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33
Q

rate: atrial 350-600, ventricular > 100
rhythm: irregualar
P wave: none-only fibulatory waves
PR interval: not measurable
QRS: ,0.12, constant

A

Atrial fibrillation

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34
Q
  • rheumatic heart disease
  • CAD
  • cardiomyopathy
  • HF
  • Pericarditis
  • thyrotoxicosis
  • alcohol intoxication
  • caffiene use
  • electrolyte disturbance
  • cardiac surgery
  • clinically associated with what rhythm
A

atrial fibrillation

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35
Q
  • Supportive treatment: oxygen
  • Medications: digoxin, Beta-blocker, Calcium channel blockers, anticoagulants, antiplatelet agents
  • Cardioversion
  • Radiofrequency catheter ablation
  • Maze procedure
  • Bi-Ventricular pacing
A

Atrial Fibrillation treatment

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36
Q

Synchronized circuit delivers a countershock on the R wave of the QRS complex of the ECG

A

cardioversion

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37
Q

Electrode-tipped catheter “burns” accessory pathways or ectopic sites in the atria, AV node, and ventricles

A

radiofrequency catheter ablation

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38
Q

Rhythm: regular or irregular
Rate: atria 240-400; ventricle rate varies (usually >120)
P wave: see flutter or “sawtooth” waves; no P wave
PR interval: not measurable
QRS:, 0.12

A

Atrial flutter

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39
Q

another name for sawtooth (flutter) waves

A

F waves

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40
Q
  • CAD, HTN, mitral valve disorders, pulmonary embolus, chronic lung disease, cardiomyopathy, hyperthyroidism
    drugs: Digoxin, quinidine, epinephrine
  • clinical associations with
A

clinical associations with atrial flutter

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41
Q
  • Supportive: Oxygen
  • medications; digoxin, beta blockers, calcium channel blockers, anticoagulants, antiplatelet agents
  • cardioversion
  • radiofrequency catheter ablation
  • Maze procedure
  • Bi-ventricular pacing
  • all treatment for*
A

Atrial flutter treatment

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42
Q
  • can occur at any rate
  • rhythm: regular but interrupted
  • Pwaves: not seen with PVC
  • PR interval: not measured
  • QRS: wide, bizarre shape, >0.12
A

premature ventricular contraction

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43
Q

types of pvc’s

A

unifocal, multifocal (more than one set is firing, look different from each other), couplet, bigeminy, trigeminy, quadrigeminy

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44
Q

trigeminy

A

2 normal qrs’s followed by a pvc

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45
Q

quadrigeminy

A

3 normal qrs’ followed by a pvc

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46
Q

stimulants: caffeine, alcohol, nicotine, aminophylline, epinephrine, isoproterenol
- digoxin
- electrolyte imbalance
- hypoxia
- fever
- Disease states: MI, mitral valve prolaps, HF, CAD
* clinical associations with which rhythm

A

PVC’s clinical association

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47
Q
  • often no treatment is required
  • Increased frequency–> treat cause
    • electrolyte replacement (K+/Mg+)
    • oxygen support
  • Suppress ventricular irritability (rapid rate)
    • amiodarone, Procainamide, Lidocaine
    • Beta blockers
  • treatment for which rhythm
A

PVC treatment

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48
Q

run of 3 or more PVC’s in a row

A

V-tach

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49
Q 
rate: 100-250
Rhythm: regular
p waves/PR interval: non identifiable
QRS: wide, bizarre, > 0.12
Cause: heart disease, injury, tissue ischemia, hypoxia, drug toxicity, electrolyte abnormalities
*rhythm?
A

ventricular tachycardia

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50
Q
  • clinical associations of?*

- Mi, CAD, electrolyte imbalance, cardiomyopathy, mitral valve prolapse, long QT syndrome, digitalis toxicity

A

V-tach clinical associations

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51
Q

treatment
-Acute: amiodarone, lidocaine, procainamide, sotalol, synchronized cardioversion, pacemaker
-Chronic:
sustained
-IV amiodarone, sotalol, ICD
non-sustained (3 or more,

A

V-tach treatment for acute and chronic

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52
Q

rate, Pwave, PR interval, QRS: not detectable

rhythm: none
causes: drowning, drug overdoses, accidental electric shock

A

ventricular fibrillation

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53
Q
  • clinical associations for?*
  • acute MI, CAD, cardiomyopathy
  • Cardiac pacing or cardiac catheterization
  • may occur with coronary re-perfusion after fibrinolytic therapy
  • accidental electric shock, hyperkalemia, hypoxia, acidosis, drug toxicity
A

V-fib clinical associations

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54
Q

treatment: initiate a code, stat defib, CPR, oxygen
meds: epi, vasopressin, amiodarone, procainamide, lidocaine
* treatment for?*

A

V-fib treatment

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55
Q

no rate, rhythm, p wave, pr interval, or qrs

A

asystole

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56
Q

a notable spike right before the QRS interval

A

paced ventricular rhythm

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57
Q

types of pacemakers

A

-temporary vs. permanent
-single chamber vs. dual chamber
-A, V, AV
-Synchronous vs. Asynchronous
-demand (synchronous): whether the
pacemaker will detect or operate in
relation to the patient’s own heart
rhythm.
-ex: will initiate and impulse on demand
if pts’s heart rhythm drops below a
set rate

-fixed (asynchronous): ignores what the
pts heart is doing. It will deliver
whatever rate it is set at no matter
what

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58
Q

designed to treat patients with chronic heart problems in which the heart beats too slowly to adequately support circulation needs, pacing leads in both the atrium and ventricle

A

permanent pacemaker, dual chamber

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59
Q
  • failure to recognize spontaneous atrial or ventricular activity and pacemaker fires inappropriately
  • lead damage, battery failure, dislodgment of electrode
A

pacemaker failure to sense

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60
Q
  • electrical charge to myocardium is insufficient to produce atrial or ventricular contraction
  • lead damage, batter failure, dislodgment of the electrode, fibrosis at the electrode tip
A

pacemaker failure to capture

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61
Q

atrial spike followed by a P qrs T

A

atrial paced rhythm

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62
Q

pacemaker spike followed by a p wave, another pacemaker spike, QRS and T

A

AV paced rhythm

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63
Q
  • a narrowing or obstruction of one or more coronary arteries as a result of atherosclerosis
  • causes decreased perfusion of myocardial tissue and inadequate myocardial oxygen supply
A

CAD

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64
Q

CAD non-modifiable risk factors

A

age, gender, family history and genetics

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65
Q

HTN, tobacco use, sedentary lifestyle, dyslipidemia, obesity, diabetes, stress, homocysteine
modifiable risk factors of?

A

-CAD modifiable risk factors

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66
Q
  • clinical manifestations*

- asymptomatic, chest pain, palpitations, diaphoresis, dyspnea, syncope, excessive fatigue

A

CAD clinical manifestations

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67
Q

EKG: ST segment depression, T wave inversion

  • Cardiac catheterization
  • Blood lipid levels: Total cholesterol, high density lipoproteins, low density lipoproteins, triglycerides
A

CAD diagnostic tools

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68
Q

meds: antilipemics, anticoagulants, ASA, ACE inhibitors, B-blockers, Calcium Channel Blockers, Nitrates

A

Medications for CAD

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69
Q
  • Angioplasty, Atherectomy, CABG, Coronary laser therapy, vascular stent
  • collaborative management for?
A

CAD collaborative managements

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70
Q

collapsed balloon catheter threaded into artery with plaque build up then dilated is what type of surgery for CAD?

A

Angioplasty

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71
Q

collapsed balloon catheter and stent threaded into artery with plaque, both are expanded, the stent is left.
Type of surgery for CAD?

A

Stent

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72
Q

catheter threaded into artery with plaque, suctions up the plaque and the device is then removed

A

Atherectomy

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73
Q

a graft is used to bipass the blocked vessel. Type of CAD surgery?

A

CABG

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74
Q
  • Myocardial 02 demand is greater than 02 supply
  • w/in minutes conversion to anaerobic metabolism
  • 30-60 minutes=myocardial damage
  • causes increased myocardial work load and obstruction of coronary artery
  • what causes all of this?
A

myocardial ischemia

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75
Q

etiology: CAD
manifestation: stable angina
- may progress to acute coronary syndromes: unstable angina, non ST elevation MI, ST elevation MI

A

myocardial ischemia

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76
Q

Ischemia does not occur globally across the heart rather it is dependent upon which coronary arteries have areas of obstruction or stenosis
*type of ischemia?

A

myocardial ischemia: stable angina

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77
Q

Characteristics:

  • pain lasting 5-15 minutes
  • typically retrosternal or just to the left of the sternum
  • can radiate to left shoulder and or arm, jaw, epigastric area, between shoulder blades
  • squeezing, burning, pressure
  • mild to moderate intensity
  • relieved with rest and/or NTG
A

stable angina characteristics

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78
Q

types of acute coronary syndrome

A

unstable angina, myocardial infarction

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79
Q

etiology:

  • rupture of an unstable plaque
  • acute coronary vasoconstriction: cocaine
A

unstable angina

80
Q
  • acute onset
  • triangle in the predictability
  • clinical presentation: symptoms of ischemia at rest, new onset of exertional angina accompanied by marked limitation of physical activity
  • EKG changes: ST depression or T wave inversion
A

unstable angina

81
Q 
diagnostic tools for ?
-EKG: T wave inversion, transient ST depression
-cardiac enzymes
-exercise stress test
stress echocardiogram
-coronary angiogram
-cardiac catheterization
A

unstable angina diagnostic tools

82
Q

Meds:

morphine sulfate, O2, nitro, beta blockers, CA+ channel blockers, platelet inhibiting agents

A

angina treatment

83
Q
  • inability of heart to pump blood to meet metabolic needs of the body
    • impaired filling (diastolic)
    • impaired pumping (systolic)
  • cardiac output diminishes
  • causes insufficient perfusion of body tissues with vital oxygen and nutrients
A

Heart failure

84
Q

precipitating factors for?

CAD/MI, dysrhythmias, infection, valve disorders, HTN, hypervolemia, hyperthyroidism, pulmonary embolism, anemia

A

HF precipitating factors

85
Q

the ability of the heart to increase cardiac output during increased activity

A

cardiac reserve

86
Q

during heart failure what happens to cardiac reserve?

A

cardiac reserve is lost during this

87
Q
  • decreased contractility of either right or left ventricle

- ejection fraction

A

systolic heart failure

88
Q
  • increased workload = hypertrophy
  • short term effect= improved contractility and cardiac output
  • long term effects; ventricular remodeling with decreased chamber size, reduced diastolic filling, increased ventricular wall tension, myocardial ischemia
A

myocardial hypertrophy

89
Q

Increased afterload is most commonly caused by ?

A

Most commonly caused by increased peripheral resistance

-ex: HTN, Aortic disease

90
Q

?—> increased catecholamine activity (epinephrine and norepinephrine)—> arterial and venous vasoconstriction

A

Increased SNS activity causes this

91
Q

Arterial effects of increased SNS activity

A
  • redistribution of blood flow: Increased BP, decreased perfusion of less metabolically active organs (kidneys, skin, GI tract) stimulate SNS
  • increased perfusion of the heart and brain
92
Q

RAAS components

A

Renin, angiotensin II, aldosterone, ADH

93
Q

Decreased renal blood flow—> increased Renin secretion which causes angiotensin II to be released. This causes two things

1: vasoconstriction, increased tissue perfusion and afterload
2: aldosterone–>retention of sodium and water—>increased venous return—>increased ventricular volume and stretch—>increased preload

A

Activation of the RAAS

94
Q

Major stretch receptors?

A

Aorta, Carotid sinus

95
Q

the Aorta and Carotid sinus are sensitive to?

A

Arterial pressure

96
Q

Natriuretic peptides

A

Atrial natriuretic peptide (ANP), Brain or B-type natriuretic peptide (BNP)

97
Q

increased angiotensin and aldosterone–>inflammatory process–>macrophage activation—>fibroblast growth and deposition of collagen—>myocardial hypertrophy and remodeling

A

inflammatory mediators

98
Q

Etiology: Ischemic heart disease, cardiomyopathy, valvular insufficiency or stenosis, anemia, HTN
- Decreased cardiac output (EFredistribution of blood to the brain and heart–>decreased peripheral tissue perfusion

A

Left Sided systolic failure

99
Q

Clinical manifestations r/t

  • decreased cardiac output
  • decreased tissue perfusion
  • vascular congestion

Increased ventricular pressure–>increased atrial pressure–>increased venous pressure–>increased capillary pressure and vascular oncotic pressure–>interstitial fluid and increased lymph drainage

A

left sided diastolic failure manifestations

100
Q

Tachycardia, a. fib., thready pulse, pulsus alternans, s3 heart sound (ventricular gallop)

A

left sided systolic failure clinical manifestations

101
Q

clinical manifestations renal:
-decreased GFR, increased BUN/Creatinine, dilutional hyponatremia, decreased urine sodium, increased urine specific gravity

Neurological (late)
-confusion, insomnia

A

left sided systolic failure renal and neurological clinical manifestations

102
Q

Diastolic dysfunction:

  • decreased left ventricular compliance (ie: increased stiffness)
  • decreased size of ventricle
  • normal ejection fraction

Etiology:

  • ischemic heart disease
  • hypertrophic cardiomyopathy
  • ventricular remodeling
  • mitral valve stenosis

Clinical Manifestations r/t:

  • increased left ventricular end-diastolic pressure
  • vascular congestion
A

Impaired filling etiology, clinical manifestations, diastolic dysfunction

103
Q

Etiology:

  • hypertension-induced myocardial hypertrophy
  • myocardial ischemia: ventricular remodeling
  • cardiomyopathy
  • Aortic or Mitral valve dysfunction
  • diabetes can increase risk
A

left sided diastolic failure etiology

104
Q

Increased ? ventricular pressure–> increased ? atrial pressure–>pulmonary venous congestion–>interstitial pulmonary edema

A

“Left”, left sided diastolic failure

105
Q

Dyspnea progressing to pulmonary edema:

  • increased work of breathing
  • dyspnea on exertion (DOE)
  • Orthopnea (difficulty sleeping)
  • paroxysmal nocturnal dyspnea (PND)
  • nonproductive cough
  • Crackles and pink frothy sputum
A

Left sided diastolic failure clinical manifestations

106
Q

Increased ? ventricular pressure—>blood backs up into ? atrium increasing ? atrial pressure–>blood backs up into venous system resulting in venous congestions

A

“right”, right sided systolic failure

107
Q

etiology:

  • left-sided heart failure
  • end stage lung disease “cor-pulmonale”
  • pulmonic or tricuspid value dysfunction
    • stenosis or regurgitation
  • right ventricle myocardial infarction
A

right sided systolic failure etiology

108
Q

right sided vs. left sided hf

A

Right:
congestion of peripheral tissues causes three things:
1. Dependent edema and ascites
2.GI tract congestion–> anorexia, GI distress, weight loss
3. Liver congestion–> signs related to impaired liver function

Left:

  • Decreased cardiac output —>activity intolerance and signs of decreased tissue perfusion
  • pulmonary congestion which causes two things:
    1. impaired gas exchange–>cyanosis and signs of hypoxia
    2. Pulmonary edema—>cough with frothy sputum, orthopnea, paroxysmal nocturnal dyspnea
109
Q

Clinical manifestations r/t:

  • decreased cardiac output
  • vascular congestion
A

combined systolic and diastolic failure clinical manifestations

110
Q

Class 1 HF

A

normal activities do not trigger symptoms

111
Q

Class 2 HF

A

ordinary activities result in fatigue, palpitations, dyspnea, angina

112
Q

Class 3 HF

A

less than ordinary activities result in symptoms

113
Q

Class 4 HF

A

Symptoms at rest

114
Q

Pulmonary Congestion:

  • hacking cough, worse at night
  • dyspnea, orthopnea
  • adventitious breath sounds
  • frothy, pink tinged sputum
  • tachypnea
  • ventricular gallop (S3)

Decreased CO

  • fatigue
  • weakness
  • oliguria during day
  • angina
  • confusion, restlessness
  • dizziness
  • tachycardia, palpitations
  • pallor
  • cool extremities
  • weak peripheral pulses
A

Left HF assessment parameters

115
Q

Systemic Congestion:

  • JVD
  • Hepatomegaly, splenomegaly
  • anorexia and nausea
  • dependent edema
  • swollen hands and fingers
  • polyuria at night
  • weight gain
  • HTN (from excess volume) or Hypotension (from failure)
A

Right Heart Failure assessment parameters

116
Q 
CXR: reveals cardiomegaly and vascular congestion
Echocardiogram reveals:
-decreased ventricular function
-decreased ejection fraction
     -left systolic failure ,40%

Elevated BNP>100
C-reactive protein (CRP

Labs:

decreased: CL, RBC’s, PsO2
increased: K, BUN, Creatinine, LFTs

A

HF diagnostic tests

117
Q

HF multisystem effects: cardiovascular, respiratory, musculoskeletal, gastrointestinal

A 
Cardiovascular:
-angina, dysrhythmias, shock, and death
Respiratory:
-pulmonary edema, pneumonia, pleural effusions
musculoskeletal:
-fatigue, weakness
Gastrointestinal:
-Anorexia, nausea, liver engorgement
118
Q

HG multisystem effects: Neurological, integumentary, genitourinary, metabolic process

A 
Neurological
-confusion, anxiety, restlessness
Integumentary
-pallor, diaphoresis, breakdown
Genitourinary
-decreased urine output, nocturia
Metabolic Process
-metabolic acidosis
119
Q
  • nursing dx interventions*
  • monitor respiratory and oxygenation status
  • Administer oxygen, as prescribed (usually if
A

Impaired gas exchange nursing dx interventions

120
Q

nursing dx interventions
Diet modifications:
-small, frequent meals, low sodium, minimize processed foods, caffeine, cholesterol and fats

A

Decreased cardiac output nursing dx interventions

121
Q

Pharm management of ? nursing dx

  • ace inhibitors
  • diuretics
  • Human B-type natriuretic peptides (BNP)
  • nitrates
  • inotropics: dig, beta-adrenergic agonists, phosphodiesterase inhibitors, calcium sensitizers
  • Beta-adrenergic blockers
A

Decreased cardiac output nursing dx pharm interventions

122
Q

Decreased cardiac output non-surgical and surgical management

A 
Nonsurgical management:
-CPAP, Cardiac resynchronization therapy
Surgical:
-Ventricular assist devices
-heart transplant
123
Q

-Chronic disease of the arteries characterized by:abnormal thickening and hardening of the vessel walls

A

arteriosclerosis

124
Q

deposits of intra-arterial fat and fibrin in the vessel walls that harden over time
-risk factors: genetics, risk factors, endothelial injury

A

atherosclerosis

125
Q

Modifiable atherosclerosis risk factors

A
  • hyperlipidemia
  • HTN
  • current cigarette smoking
  • type II diabetes
  • increased homocysteine, lipoprotein a, and high sensitivity C-reactive protein (CRP)
126
Q

Contains:

  • lipid filled macrophages: foam cells
  • cholesterol deposits
  • necrotic cellular debris
  • lipids
  • fibrous covering/cap
A

atheromatous plaques

127
Q

Attachment of monocytes to damaged vascular endothelium–>migration of the monocyte into the subendothelial layer–>monocyte transforms into macrophage–>macrophage engulf lipoproteins (LDL)—>activated macrophages release toxic oxygen species oxidized LDL–>oxidized LDL engulfed by macrophages: foam cells

A

formation of atheromatous plaques

128
Q

Continuing vessel wall damage–>when lesion becomes unstable–>plaque rupture–>platelet adhesion and clotting cascade–>formation of thrombus–>occlussion–>ischemia–>infarction

A

formation of atheromatous plaques

129
Q
  • able to identify cause and correct
  • precipitating disorders or conditions:
  • renal disorders, cardiovascular disorders, endocrine disorders, neurogenic disturbances, medications
A

secondary HTN

130
Q

SNS pathogenesis:

  • development and continuance of increased BP:
  • role in end organ damage
  • increased HR and systemic vasoconstriction/increased BP
  • vascular remodeling
  • renal sodium retention
  • insulin resistance
  • increased renin and angiotensin levels
A

SNS pathogenesis of secondary HTN

131
Q

Angiotensin II mediates ?

A

mediates arteriolar remodeling

-changing structure and function of vessel wall, increased peripheral resistance

132
Q

Aldosterone causes?

A

causes sodium retention

133
Q

Can either cause diuresis, or increase the vascular tone of the blood vessels if they are not functioning properly

A

natriuretic peptides and HTN

134
Q

Endothelial injury and ischemia

  • release of inflammatory cytokines
  • vascular remodeling and smooth muscle contraction
  • decrease in vasodilators (nitric oxide)
  • increase in vasoconstrictors (endothelin)
A

pathogenesis: inflammation and HTN

135
Q
  • cardiovascular damage
  • peripheral vascular damage
  • target “end” organ damage
  • can all be caused by
A

*can all be caused by HTN

136
Q
  • Accelerated atherosclerosis
  • decreased myocardial oxygen supply
  • risk myocardial infarction
  • Increased resistance to LV ejection (systole)
  • increased cardiac workload
  • LV hypertrophy–> increased cardiac output
  • LV dilation and failure
  • Cardiovascular repercussions of ?
A

Cardiovascular repercussions of HTN

137
Q
  • Structural changes in small arteries and arterioles from ?
  • narrowing of vascular lumen
  • decreased arterial flow
  • tissue microinfarction
  • organ dysfunction
  • aneurysms
A

peripheral vascular damage of HTN

138
Q

abnormal drop in BP with the assumption of an upright position

  • Decreased SBP greater than or equal to 20mm HG
  • decreased DBP greater than or equal to 10 mm HG
A

orthostatic hypotension definition

139
Q

etiology:

-hypovolemia, anti-hypertensive drugs, aging, prolonged bedrest

A

orthostatic hypotension etiology

140
Q
  • Localized dilation of the arterial wall
  • atrophy of the medial layer of the artery
  • Location
  • aorta: abdominal and thoracic
  • femoral
  • cerebral
A

Complication of HTN: Aneurism

141
Q

clinical manifestations are often none until rupture

A

Aneurysm clinical manifestations

142
Q

pulsatile mass to the left of the umbilicus, problems with lower extremities being cool, mottled, pale, cyanotic, pain

A

abdominal aneurism physical assessment

143
Q

dysphagia r/t compression of the esophagus, cough, difficulty breathing, back pain which is worse when laying down

A

thoracic aneurism clinical assessment

144
Q

Sudden, severe and persistent pain described as “tearing” or “ripping” in anterior chest and or back

S/S

  • pallor, sweating, tachycardia,
  • different B/P in each arm
  • paralysis of lower extremities
  • SHOCK, SHOCK, SHOCK
A

Aortic dissection definition and S/s

145
Q
  • nursing actions for?*
  • maintain bed rest with legs flat; avoid crossing legs
  • maintain calm environment
  • prevent straining during defection
  • instruct to avoid holding breath when moving
  • administer beta-blockers, antihypertensives
  • monitor EKG; VS, urine output
A

Nursing actions to prevent aneurysm rupture

146
Q

2 surgical procedures done for aneurysm

A

-Open surgical procedure: excise aneurism and replace with synthetic graft
Endovascular stent grafts
-Stent, metal sheath covered with polyester fabric is placed percutaneously under fluroscopy

147
Q

Aneurysm surgical complications post op (6)

A
  • renal failure
  • graft occlusion
  • respiratory distress
  • cardiac arrhythmias
  • paralytic ileus
  • sepsis
148
Q

Arterial thrombosis or embolism; abrupt onset

A

Acute peripheral artery disease

149
Q

Peripheral arteriosclerosis, occurs over time

A

Chronic peripheral artery disease

150
Q

Acute arterial occlusion results in?

A
  • results in:

- tissue ischemia, risk for necrosis, risk for gangrene

151
Q
  • Blood clot on vessel wall
  • develop where intravascular factors stimulate coagulation
  • also could relate to infection or inflammation or pooling of blood
  • if coagulation occurs, thrombus forms
  • thrombus can occlude artery
A

arterial thrombosis

152
Q
  • sudden obstruction; blood clots floating in the circulating blood, usually originates in the heart and become lodged in a vessel too small to accommodate its passage
  • associated with: MI, valvular disease, left-soded heart failure, atrial fib
A

arterial embolism

153
Q

6 P’s assessed for in arterial thrombosis and embolis

A
  • sudden or insidious pain in region affected
  • numbness of affected extremity (polar)
  • pallor or mottling of skin in affected extremity
  • pulselessness
  • possible paralysis
  • possible line of demarcation,cool or cold skin
154
Q

Confirms arterial occlusion dx, locates occlusion, extent of occlusion, dx based on s/s

A

arteriography

155
Q

Arterial occlusion meds and surgery

A

meds:
-anticoagulants and thrombolytic therapy
Surgery:
-thrombectomy (coil inserted tool around thrombus and pull it back out), embolectomy, thromboendarterectomy (open the vessel up and pull it out)

156
Q
  • nursing actions for ?*
  • maintain IV fluids as ordered
  • protect extremity, no heat or cold, bed cradle
  • keep extremity horizonal
  • no knee gatch, pillows under extremity, or sitting with 90 degree hip flexion
A

Ineffective tissue perfusion management of blockage of blood flow

157
Q
  • clinical manifestation for?*
  • intermittent claudication (pain that they feel in their extremities is brought on by exercise)
  • rest pain-paresthesias (numbness, decreased sensation)
  • diminished or absent peripheral pulses
  • pallor with extremities elevated, dependent rubor when dependent
  • thin, shiny, hairless skin, thickened toenails
  • area of discoloration or skin breakdown
A

Peripheral atherosclerosis clinical manifestations

158
Q

5 peripheral atherosclerosis complications

A

Gangrene, extremity amputation, rupture of AAA, infection, sepsis

159
Q

Evaluates oxygenation of tissues

A

transcutaneous oximetry

160
Q

injection of radiopaque contrast medium into an artery with the same nursing implications as coronary ?

A

Angiography

161
Q
  • client education with ?*
  • lose weight and eat low fat, cholesterol, and sodium diet
  • do not stand or sit for long periods of time
  • notify healthcare provider or any changes in color, sensation, temperature, or pulses in extremities
  • medication side effects-bleeding (GI)
A

Client education with PAD

162
Q

Bipass graft post-surgical care (4)

A
  • assess 6 p’s of ischemia
  • no hip or knee bending
  • bedrest 1st 24 hours
  • keep hydrated with IV fluids
163
Q
  • Aspirin
  • Plavix (clopidogrel)
  • Ticlid (ticlopidine) (improves microviscosity)
  • Trental (pentoxyfylline)
  • Pletal (cilostazol) (platelet inhibitor, promotes vasodilation)
A

Medication for PAD

164
Q

Other word for Buerger’s disease

A

aka thrombangitis obliterans

165
Q
  • inflammatory response in medium and small arteries and veins of the hands and feet
  • unknown etiology; directly r/t smoking, young men
  • characterized by intermittent claudication of the arches of the foot, sensitivity to cold, numbness, diminished pulses, red or cyanotic extremities in dependent position, ulcerations
A

Beurger’s (thrombangitis obliterans) disease

166
Q

(4) Beurger’s disease collaborative management

A

-smoking cessation, prevent vasoconstriction, improve peripheral blood flow, prevent complications

167
Q

Raynaud’s Disease vs. Raynauds phenomenon

A

Phenominon: no idea what’s causing it, often confined to the hands

168
Q

Vasospasm of the small arteries of the upper and lower extremities, predominantly the hands

  • “white-blue-red disease”
  • other s/s: numbness, stiffness, decreased sensation, aching pain
  • primarily affect young women
A

Raynaud’s disease

169
Q

Cold or stress–>Activation of the sympathetic nervous system–>peripheral arterial vasospasm–>decreased blood flow

A

Reynaud’s disease cold or stress

170
Q

Reynauds disease medicine

A

calcium channel blockers, vascular smooth muscle relaxants, vasodilators

171
Q

Blood clot forms on wall creating some obstruction. Form in superficial or deep veins

A

venous thrombosis

172
Q
  • risk factors for?*
  • immobilization
  • surgery
  • cancer
  • trauma
  • pregnancy
  • hormone therapy
  • coagulation disorders
A

venous thrombosis risk factors

173
Q
  • clinical manifestations for?*
  • dull, aching pain over affected vein
  • marked redness along the course of the vein
  • increased warmth over area of inflammation
  • palpable cord like structure
A

superficial thrombophlebitis clinical manifestations

174
Q

Blood clot found in the veins of the lower extremities

A

Deep vein thrombosis (DVT)

175
Q
  • risk factors for?*
  • marked immobility
  • dehydration
  • advanced malignancy
  • varicose veins
  • pelvic trauma or surgery
  • leg trauma or surgery
A

risk factors for DVT

176
Q

Virchow Triad

A

Triangle with thrombosis in the middle and circulatory statis, endothelial injury, and hypercoagulability state

177
Q

clot formation–>venous obstruction–>venous pooling–>increased intravascular volume–>interstitial edema

A

DVT pathogenesis

178
Q
  • clinical manifestations for?*
  • dull, aching pain in affected extremity, especially when walking
  • cyanosis of affected extremity
  • warmth of affected extremity
  • general malaise
A

DVT clinical manifestations

179
Q

4 types of thrombophlebitis medications

A
  • anti-coagulants (heparin, coumadin)
  • antiplatelets
  • thrombolytics
  • analgesics
180
Q

Thrombophlebitis nursing actions for pain (3) and decreasing edema (3) prevent skin ulceration (1) prevent pulmonary emboli (3)

A

*Provide pain relief
-assess pain scale 1-10
-elevate affected leg higher than heart
-administer analgesics
*Decrease edema
-Apply warm, moist compress, intermittent or continuous to affected extremity
-measure/monitor leg/arm circumference
-monitor neurovascular status-especially
peripheral pulses
*Prevent skin ulcerations
-keep bed covers/clothing from touching affected limb
*Prevent pulmonary emboli
-maintain strict bedrest
-never massage affected extremity-may release clot
-monitor HR/RR

181
Q

3 surgical interventions for thrombophlebitis

A
  • venous thrombectomy
  • vena cava filter
  • ligation or plication
182
Q

PH
Pt
INR

A

ptth-heparin
PTT-coumadin
INR- between 2 and 3 if they are having a therapeutic response to coumadin

183
Q

lovenox and fragmin

A

low molecular weight heparins (anticoagulants), don’t need to be monitoring the blood levels because they tend to be more predictable in terms of the metabolism of the drug

184
Q

reopro, agrastat, integrilin

A

anticlotting agents

185
Q

TPA, reteplase

A

thrombolytics

186
Q

thrombolytics most affective when administered within?

A

5 days

187
Q

Pts. on anticoagulant therapy are recommended to not use what type of medication?

A

aspirin containing products

188
Q

Pts. on anticoagulation therapy are advised to avoid what kind of foods?

A

Avoid foods high in vitamin K

189
Q

inadequate venous return over a prolonged period of time

  • Causes: DVT, varicose veins, leg trauma
  • Results in venous stasis: incompetent valves, ineffective muscle-pumping action to propel blood back to heart
A

Chronic venous insufficiency

190
Q
  • Clinical manifestations of ?*
  • lower leg edema
  • brownish discoloration of the skin of the lower leg and foot
  • itching
  • hardness of subcutaneous tissues
  • stasis ulcers over the ankle
A

Chronic venous insufficiency clinical manifestations

191
Q

Arterial vs. Venous insufficiency

  • pulses
  • hair distribution
  • nails
  • skin
  • neurologic
  • edema
A
  • Arterial
  • Pulses: absent
  • Hair distribution: loss
  • Nails: thick
  • Skin: Think, shiny, rubor on dependency
  • Neurologic: sensory loss
  • Edema: worse with elevation

Venous

  • Pulses: present
  • Hair distribution: no loss
  • Nails: black, brownish
  • Skin: rough, brown pigment, cyanosis on dependency
  • Neurologic: no loss
  • Edema: improves with elevation
192
Q

Dilated, elongated branches of veins resulting from incompetent valves, venous insufficiency, heredity or long standing

  • dx:visual inspection, venous doppler
  • Complication: DVT
A

Varicose veins

193
Q

Elevated venous pressure–>valve incompetence–>reflux of blood–>venous distention

A

varicose veins pathogenesis

194
Q

Laser therapy is very affective for?

A

Varicose vein treatment

195
Q

Unna boot

A

for venous stasis ulcer treatment

-helps form sterile & moist environment, stays in place 1-2 weeks and is changed

BEACON MedSurg/Peds (21 decks)

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