Test 3 Perfusion Flashcards
1
Q
4 unique components of cardiac cells
A
conductivity, excitability, automaticity, contractility
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
3
Q
60-100 beats per minute conduction origination
A
SA node
4
Q
40-60 beats per minute conduction origination
A
AV node
5
Q
Ventricle 20-40 beats per minute conduction origination
A
Ventricle
6
Q
horizontal lines on the EKG paper measure
A
force of the electrical impulse is measured by amplitude (voltage)
7
Q
verticle lines in EKG
A
measure time
8
Q
.04 seconds on EKG=
A
small square
9
Q
0.2 seconds on EKG strip =
A
heavy line, or 5 small squares
10
Q
1 second on EKG strips =
A
5 large squares
11
Q
1 minute =
A
3 hatch marks
12
Q
P wave form represents
A
atrial depolarization (contractions) and emptying of the right and left atria
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)
14
Q
QRS complex represents
A
ventricular depolarization, an electrical activity that causes both ventricles to contract and send blood out into the body
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
16
Q
T wave
A
follows ST segment, represents ventricular repolarization
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
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
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
20
Q
Step 4 EKG analysis
A
- Determine regularity-is it regular, regular but interrupted, or irregular
- compare r-r intervals
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
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)
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
24
Q
rate: <0.12
A
Sinus Bradycardia
25
in response to sinus brady interventions
carotid sinus massage, hypothermia, increased vagal tone, administration of parasympathomimetic drugs
26
hypothyroidism, increased intracranial pressure, obstructive jaundice, inferior wall MI
* all disease states causing which rhythm?
disease states with sinus brady
27
dizziness or syncope, weakness, pallor, diaphoresis, hypotension, angina, confusion, SOB
*all indicate
sinus brady
28
treatment of sinus brady
oxygen, atropine, pacemaker, additional medications
29
rate: 100-160, rhythm, p wave, pr and qrs interval are normal
sinus tachy
30
exercise, emotional stress, fever, pain, hypovolemia, anemia, myocardial ischemia, HG, thyrotoxicosis, EtOH/EtOH withdrawal
*all clinical associations with which rhythm
sinus tachy
31
hypotension, lightheadedness, palpitations, chest pain, restlessness, anxiety
*symptoms of
sinus tachy
32
- oxygen
- beta-adrenergic blockers
- analgesics
- antipyretics and antibiotics
- diuretics and inotropic agents
- fluid replacement
* all treatments done for which rhythm
sinus tachy
33
rate: atrial 350-600, ventricular > 100
rhythm: irregualar
P wave: none-only fibulatory waves
PR interval: not measurable
QRS: ,0.12, constant
Atrial fibrillation
34
- rheumatic heart disease
- CAD
- cardiomyopathy
- HF
- Pericarditis
- thyrotoxicosis
- alcohol intoxication
- caffiene use
- electrolyte disturbance
- cardiac surgery
* clinically associated with what rhythm
atrial fibrillation
35
- Supportive treatment: oxygen
- Medications: digoxin, Beta-blocker, Calcium channel blockers, anticoagulants, antiplatelet agents
- Cardioversion
- Radiofrequency catheter ablation
- Maze procedure
- Bi-Ventricular pacing
Atrial Fibrillation treatment
36
Synchronized circuit delivers a countershock on the R wave of the QRS complex of the ECG
cardioversion
37
Electrode-tipped catheter "burns" accessory pathways or ectopic sites in the atria, AV node, and ventricles
radiofrequency catheter ablation
38
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
Atrial flutter
39
another name for sawtooth (flutter) waves
F waves
40
- CAD, HTN, mitral valve disorders, pulmonary embolus, chronic lung disease, cardiomyopathy, hyperthyroidism
drugs: Digoxin, quinidine, epinephrine
* clinical associations with
clinical associations with atrial flutter
41
- Supportive: Oxygen
- medications; digoxin, beta blockers, calcium channel blockers, anticoagulants, antiplatelet agents
- cardioversion
- radiofrequency catheter ablation
- Maze procedure
- Bi-ventricular pacing
* all treatment for*
Atrial flutter treatment
42
- can occur at any rate
- rhythm: regular but interrupted
- Pwaves: not seen with PVC
- PR interval: not measured
- QRS: wide, bizarre shape, >0.12
premature ventricular contraction
43
types of pvc's
unifocal, multifocal (more than one set is firing, look different from each other), couplet, bigeminy, trigeminy, quadrigeminy
44
trigeminy
2 normal qrs's followed by a pvc
45
quadrigeminy
3 normal qrs' followed by a pvc
46
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
PVC's clinical association
47
- 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
PVC treatment
48
run of 3 or more PVC's in a row
V-tach
49
```
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?
```
ventricular tachycardia
50
* clinical associations of?*
| - Mi, CAD, electrolyte imbalance, cardiomyopathy, mitral valve prolapse, long QT syndrome, digitalis toxicity
V-tach clinical associations
51
*treatment*
-Acute: amiodarone, lidocaine, procainamide, sotalol, synchronized cardioversion, pacemaker
-Chronic:
sustained
-IV amiodarone, sotalol, ICD
non-sustained (3 or more,
V-tach treatment for acute and chronic
52
rate, Pwave, PR interval, QRS: not detectable
rhythm: none
causes: drowning, drug overdoses, accidental electric shock
ventricular fibrillation
53
* 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
V-fib clinical associations
54
treatment: initiate a code, stat defib, CPR, oxygen
meds: epi, vasopressin, amiodarone, procainamide, lidocaine
* treatment for?*
V-fib treatment
55
no rate, rhythm, p wave, pr interval, or qrs
asystole
56
a notable spike right before the QRS interval
paced ventricular rhythm
57
types of pacemakers
-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
58
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
permanent pacemaker, dual chamber
59
- failure to recognize spontaneous atrial or ventricular activity and pacemaker fires inappropriately
- lead damage, battery failure, dislodgment of electrode
pacemaker failure to sense
60
- 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
pacemaker failure to capture
61
atrial spike followed by a P qrs T
atrial paced rhythm
62
pacemaker spike followed by a p wave, another pacemaker spike, QRS and T
AV paced rhythm
63
- 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
CAD
64
CAD non-modifiable risk factors
age, gender, family history and genetics
65
HTN, tobacco use, sedentary lifestyle, dyslipidemia, obesity, diabetes, stress, homocysteine
*modifiable risk factors of?*
-CAD modifiable risk factors
66
* clinical manifestations*
| - asymptomatic, chest pain, palpitations, diaphoresis, dyspnea, syncope, excessive fatigue
CAD clinical manifestations
67
EKG: ST segment depression, T wave inversion
- Cardiac catheterization
- Blood lipid levels: Total cholesterol, high density lipoproteins, low density lipoproteins, triglycerides
CAD diagnostic tools
68
meds: antilipemics, anticoagulants, ASA, ACE inhibitors, B-blockers, Calcium Channel Blockers, Nitrates
Medications for CAD
69
- Angioplasty, Atherectomy, CABG, Coronary laser therapy, vascular stent
* collaborative management for?
CAD collaborative managements
70
collapsed balloon catheter threaded into artery with plaque build up then dilated is what type of surgery for CAD?
Angioplasty
71
collapsed balloon catheter and stent threaded into artery with plaque, both are expanded, the stent is left.
Type of surgery for CAD?
Stent
72
catheter threaded into artery with plaque, suctions up the plaque and the device is then removed
Atherectomy
73
a graft is used to bipass the blocked vessel. Type of CAD surgery?
CABG
74
- 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?
myocardial ischemia
75
etiology: CAD
manifestation: stable angina
- may progress to acute coronary syndromes: unstable angina, non ST elevation MI, ST elevation MI
myocardial ischemia
76
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?
myocardial ischemia: stable angina
77
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
stable angina characteristics
78
types of acute coronary syndrome
unstable angina, myocardial infarction
79
etiology:
- rupture of an unstable plaque
- acute coronary vasoconstriction: cocaine
unstable angina
80
- 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
unstable angina
81
```
diagnostic tools for ?
-EKG: T wave inversion, transient ST depression
-cardiac enzymes
-exercise stress test
stress echocardiogram
-coronary angiogram
-cardiac catheterization
```
unstable angina diagnostic tools
82
Meds:
| morphine sulfate, O2, nitro, beta blockers, CA+ channel blockers, platelet inhibiting agents
angina treatment
83
- 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
Heart failure
84
precipitating factors for?
| CAD/MI, dysrhythmias, infection, valve disorders, HTN, hypervolemia, hyperthyroidism, pulmonary embolism, anemia
HF precipitating factors
85
the ability of the heart to increase cardiac output during increased activity
cardiac reserve
86
during heart failure what happens to cardiac reserve?
cardiac reserve is lost during this
87
- decreased contractility of either right or left ventricle
| - ejection fraction
systolic heart failure
88
- 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
myocardial hypertrophy
89
Increased afterload is most commonly caused by ?
Most commonly caused by increased peripheral resistance
| -ex: HTN, Aortic disease
90
?---> increased catecholamine activity (epinephrine and norepinephrine)---> arterial and venous vasoconstriction
Increased SNS activity causes this
91
Arterial effects of increased SNS activity
- 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
RAAS components
Renin, angiotensin II, aldosterone, ADH
93
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
Activation of the RAAS
94
Major stretch receptors?
Aorta, Carotid sinus
95
the Aorta and Carotid sinus are sensitive to?
Arterial pressure
96
Natriuretic peptides
Atrial natriuretic peptide (ANP), Brain or B-type natriuretic peptide (BNP)
97
increased angiotensin and aldosterone-->inflammatory process-->macrophage activation--->fibroblast growth and deposition of collagen--->myocardial hypertrophy and remodeling
inflammatory mediators
98
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
Left Sided systolic failure
99
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
left sided diastolic failure manifestations
100
Tachycardia, a. fib., thready pulse, pulsus alternans, s3 heart sound (ventricular gallop)
left sided systolic failure clinical manifestations
101
clinical manifestations renal:
-decreased GFR, increased BUN/Creatinine, dilutional hyponatremia, decreased urine sodium, increased urine specific gravity
Neurological (late)
-confusion, insomnia
left sided systolic failure renal and neurological clinical manifestations
102
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
Impaired filling etiology, clinical manifestations, diastolic dysfunction
103
Etiology:
- hypertension-induced myocardial hypertrophy
- myocardial ischemia: ventricular remodeling
- cardiomyopathy
- Aortic or Mitral valve dysfunction
- diabetes can increase risk
left sided diastolic failure etiology
104
Increased ? ventricular pressure--> increased ? atrial pressure-->pulmonary venous congestion-->interstitial pulmonary edema
"Left", left sided diastolic failure
105
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
Left sided diastolic failure clinical manifestations
106
Increased ? ventricular pressure--->blood backs up into ? atrium increasing ? atrial pressure-->blood backs up into venous system resulting in venous congestions
"right", right sided systolic failure
107
etiology:
- left-sided heart failure
- end stage lung disease "cor-pulmonale"
- pulmonic or tricuspid value dysfunction
- stenosis or regurgitation
- right ventricle myocardial infarction
right sided systolic failure etiology
108
right sided vs. left sided hf
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
Clinical manifestations r/t:
- decreased cardiac output
- vascular congestion
combined systolic and diastolic failure clinical manifestations
110
Class 1 HF
normal activities do not trigger symptoms
111
Class 2 HF
ordinary activities result in fatigue, palpitations, dyspnea, angina
112
Class 3 HF
less than ordinary activities result in symptoms
113
Class 4 HF
Symptoms at rest
114
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
Left HF assessment parameters
115
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)
Right Heart Failure assessment parameters
116
```
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
HF diagnostic tests
117
HF multisystem effects: cardiovascular, respiratory, musculoskeletal, gastrointestinal
```
Cardiovascular:
-angina, dysrhythmias, shock, and death
Respiratory:
-pulmonary edema, pneumonia, pleural effusions
musculoskeletal:
-fatigue, weakness
Gastrointestinal:
-Anorexia, nausea, liver engorgement
```
118
HG multisystem effects: Neurological, integumentary, genitourinary, metabolic process
```
Neurological
-confusion, anxiety, restlessness
Integumentary
-pallor, diaphoresis, breakdown
Genitourinary
-decreased urine output, nocturia
Metabolic Process
-metabolic acidosis
```
119
* nursing dx interventions*
- monitor respiratory and oxygenation status
- Administer oxygen, as prescribed (usually if
Impaired gas exchange nursing dx interventions
120
*nursing dx interventions*
Diet modifications:
-small, frequent meals, low sodium, minimize processed foods, caffeine, cholesterol and fats
Decreased cardiac output nursing dx interventions
121
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
Decreased cardiac output nursing dx pharm interventions
122
Decreased cardiac output non-surgical and surgical management
```
Nonsurgical management:
-CPAP, Cardiac resynchronization therapy
Surgical:
-Ventricular assist devices
-heart transplant
```
123
-Chronic disease of the arteries characterized by:abnormal thickening and hardening of the vessel walls
arteriosclerosis
124
deposits of intra-arterial fat and fibrin in the vessel walls that harden over time
-risk factors: genetics, risk factors, endothelial injury
atherosclerosis
125
Modifiable atherosclerosis risk factors
- hyperlipidemia
- HTN
- current cigarette smoking
- type II diabetes
- increased homocysteine, lipoprotein a, and high sensitivity C-reactive protein (CRP)
126
Contains:
- lipid filled macrophages: foam cells
- cholesterol deposits
- necrotic cellular debris
- lipids
- fibrous covering/cap
atheromatous plaques
127
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
formation of atheromatous plaques
128
Continuing vessel wall damage-->when lesion becomes unstable-->plaque rupture-->platelet adhesion and clotting cascade-->formation of thrombus-->occlussion-->ischemia-->infarction
formation of atheromatous plaques
129
* able to identify cause and correct
* precipitating disorders or conditions:
- renal disorders, cardiovascular disorders, endocrine disorders, neurogenic disturbances, medications
secondary HTN
130
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
SNS pathogenesis of secondary HTN
131
Angiotensin II mediates ?
mediates arteriolar remodeling
| -changing structure and function of vessel wall, increased peripheral resistance
132
Aldosterone causes?
causes sodium retention
133
Can either cause diuresis, or increase the vascular tone of the blood vessels if they are not functioning properly
natriuretic peptides and HTN
134
Endothelial injury and ischemia
- release of inflammatory cytokines
- vascular remodeling and smooth muscle contraction
- decrease in vasodilators (nitric oxide)
- increase in vasoconstrictors (endothelin)
pathogenesis: inflammation and HTN
135
- cardiovascular damage
- peripheral vascular damage
- target "end" organ damage
* can all be caused by
*can all be caused by HTN
136
* 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 ?
Cardiovascular repercussions of HTN
137
* Structural changes in small arteries and arterioles from ?
- narrowing of vascular lumen
- decreased arterial flow
- tissue microinfarction
- organ dysfunction
* aneurysms
peripheral vascular damage of HTN
138
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
orthostatic hypotension definition
139
etiology:
| -hypovolemia, anti-hypertensive drugs, aging, prolonged bedrest
orthostatic hypotension etiology
140
* Localized dilation of the arterial wall
- atrophy of the medial layer of the artery
* Location
- aorta: abdominal and thoracic
- femoral
- cerebral
Complication of HTN: Aneurism
141
clinical manifestations are often none until rupture
Aneurysm clinical manifestations
142
pulsatile mass to the left of the umbilicus, problems with lower extremities being cool, mottled, pale, cyanotic, pain
abdominal aneurism physical assessment
143
dysphagia r/t compression of the esophagus, cough, difficulty breathing, back pain which is worse when laying down
thoracic aneurism clinical assessment
144
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
Aortic dissection definition and S/s
145
* 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
Nursing actions to prevent aneurysm rupture
146
2 surgical procedures done for aneurysm
-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
Aneurysm surgical complications post op (6)
- renal failure
- graft occlusion
- respiratory distress
- cardiac arrhythmias
- paralytic ileus
- sepsis
148
Arterial thrombosis or embolism; abrupt onset
Acute peripheral artery disease
149
Peripheral arteriosclerosis, occurs over time
Chronic peripheral artery disease
150
Acute arterial occlusion results in?
* results in:
| - tissue ischemia, risk for necrosis, risk for gangrene
151
- 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
arterial thrombosis
152
- 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
arterial embolism
153
6 P's assessed for in arterial thrombosis and embolis
- 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
Confirms arterial occlusion dx, locates occlusion, extent of occlusion, dx based on s/s
arteriography
155
Arterial occlusion meds and surgery
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
* 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
Ineffective tissue perfusion management of blockage of blood flow
157
* 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
Peripheral atherosclerosis clinical manifestations
158
5 peripheral atherosclerosis complications
Gangrene, extremity amputation, rupture of AAA, infection, sepsis
159
Evaluates oxygenation of tissues
transcutaneous oximetry
160
injection of radiopaque contrast medium into an artery with the same nursing implications as coronary ?
Angiography
161
* 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)
Client education with PAD
162
Bipass graft post-surgical care (4)
- assess 6 p's of ischemia
- no hip or knee bending
- bedrest 1st 24 hours
- keep hydrated with IV fluids
163
- Aspirin
- Plavix (clopidogrel)
- Ticlid (ticlopidine) (improves microviscosity)
- Trental (pentoxyfylline)
- Pletal (cilostazol) (platelet inhibitor, promotes vasodilation)
Medication for PAD
164
Other word for Buerger's disease
aka thrombangitis obliterans
165
- 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
Beurger's (thrombangitis obliterans) disease
166
(4) Beurger's disease collaborative management
-smoking cessation, prevent vasoconstriction, improve peripheral blood flow, prevent complications
167
Raynaud's Disease vs. Raynauds phenomenon
Phenominon: no idea what's causing it, often confined to the hands
168
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
Raynaud's disease
169
Cold or stress-->Activation of the sympathetic nervous system-->peripheral arterial vasospasm-->decreased blood flow
Reynaud's disease cold or stress
170
Reynauds disease medicine
calcium channel blockers, vascular smooth muscle relaxants, vasodilators
171
Blood clot forms on wall creating some obstruction. Form in superficial or deep veins
venous thrombosis
172
* risk factors for?*
- immobilization
- surgery
- cancer
- trauma
- pregnancy
- hormone therapy
- coagulation disorders
venous thrombosis risk factors
173
* 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
superficial thrombophlebitis clinical manifestations
174
Blood clot found in the veins of the lower extremities
Deep vein thrombosis (DVT)
175
* risk factors for?*
- marked immobility
- dehydration
- advanced malignancy
- varicose veins
- pelvic trauma or surgery
- leg trauma or surgery
risk factors for DVT
176
Virchow Triad
Triangle with thrombosis in the middle and circulatory statis, endothelial injury, and hypercoagulability state
177
clot formation-->venous obstruction-->venous pooling-->increased intravascular volume-->interstitial edema
DVT pathogenesis
178
* clinical manifestations for?*
- dull, aching pain in affected extremity, especially when walking
- cyanosis of affected extremity
- warmth of affected extremity
- general malaise
DVT clinical manifestations
179
4 types of thrombophlebitis medications
- anti-coagulants (heparin, coumadin)
- antiplatelets
- thrombolytics
- analgesics
180
Thrombophlebitis nursing actions for pain (3) and decreasing edema (3) prevent skin ulceration (1) prevent pulmonary emboli (3)
*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
3 surgical interventions for thrombophlebitis
- venous thrombectomy
- vena cava filter
- ligation or plication
182
PH
Pt
INR
ptth-heparin
PTT-coumadin
INR- between 2 and 3 if they are having a therapeutic response to coumadin
183
lovenox and fragmin
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
reopro, agrastat, integrilin
anticlotting agents
185
TPA, reteplase
thrombolytics
186
thrombolytics most affective when administered within?
5 days
187
Pts. on anticoagulant therapy are recommended to not use what type of medication?
aspirin containing products
188
Pts. on anticoagulation therapy are advised to avoid what kind of foods?
Avoid foods high in vitamin K
189
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
Chronic venous insufficiency
190
* 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
Chronic venous insufficiency clinical manifestations
191
Arterial vs. Venous insufficiency
- pulses
- hair distribution
- nails
- skin
- neurologic
- edema
* 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
Dilated, elongated branches of veins resulting from incompetent valves, venous insufficiency, heredity or long standing
- dx:visual inspection, venous doppler
- Complication: DVT
Varicose veins
193
Elevated venous pressure-->valve incompetence-->reflux of blood-->venous distention
varicose veins pathogenesis
194
Laser therapy is very affective for?
Varicose vein treatment
195
Unna boot
for venous stasis ulcer treatment
| -helps form sterile & moist environment, stays in place 1-2 weeks and is changed
