1
Q
venous insufficiency is a result of
A
- prolonged venous hypertension
- stretching veins
- damaging valves
venous stasis dermatitis or ulcers, swelling, and cellulitis
2
Q
causes of venous insufficiency
A
- standing or sitting for long periods of time
- obesity
- thrombus formation
3
Q
clinical manifestations of venous insufficiency
A
- edema of both legs
- stasis dermatitis
4
Q
goal of management for venous insufficiency
A
decreases edema and increase venous return
5
Q
nonsurgical management of venous insufficiency
A
- management of edema-leg elevation, compression stockings
- management of venous stasis ulcers
- drug therapy
6
Q
surgical management of venous insufficiency
A
not usually done because it is not successful
7
Q
varicose veins
A
distended, protruding veins that appear darkened and tortuous
- common in adults over 30 whose occupation requires prolonged standing
8
Q
conservation management of varicose veins: the 3 E’s
A
elastic stockings
elevation of extremities
exercise
9
Q
conservation management of varicose veins
A
- sclerotherapy
- surgical removal/stripping of veins
- endovenous ablation to heat the veins
- 3 E’s: elastic stockings, elevation of extremities, exercise
10
Q
desired blood pressure: people over 60
A
below 150/90
11
Q
desired blood pressure: people younger than 60
A
below 140/90
12
Q
according to the JNC 8 guidelines, patients with what BP level should be treated with drug therapy (for HTN)
A
people over 60: 150/90
people under 60: 140/90
13
Q
malignant hypertension
A
aka HTN crisis
- severe type of elevated BP that rapidly progresses, Medical Emergency
- systolic: > 180
- diastolic: > 120
14
Q
one of the most common health problems seen in primary care settings
A
hypertension
15
Q
hypertension is classified as
A
- essential (primary) or
- secondary
16
Q
essential (primary) HTN
A
no real cause; most common form
- not due to medical condition, due to risk factors: diet, sedentary, physical inactivity, smoking
17
Q
secondary HTN
A
specific disease states or drugs can increase susceptibility to HTN
- end-stage renal disease (kidney d/o)
- cushings
- pregnancy
18
Q
hypertension is called the
A
silent disease
19
Q
hypertension damages __
A
the endothelium of blood vessels
20
Q
mechanisms that influence/control blood pressure
A
- the arterial baroreceptor system
- regulation of bodily fluid volume
- the renin-angiotensin-aldosterone system
- vascular autoregulation
21
Q
essential (primary) HTN: risk factors
A
- Age greater than 60 years
- Family history of hypertension*
- Obesity
- Physical inactivity
- Excessive alcohol intake
- Hyperlipidemia
- African-American ethnicity
- High intake of salt or caffeine
- ↓Intake of K+, Ca+, or Mg+
- Smoking
- Stress
22
Q
secondary HTN: risk factors/causes
A
- Kidney disease
- Primary aldosteronism
- Pheochromocytoma
- Cushing’s syndrome
- Pregnancy
- Medications
23
Q
ABI indicative of PAD
A
ABI < 0.9
24
Q
ABI formula
A
highest systolic pressure from leg
divided by
highest systolic pressure from brachia
25
how ABI is calculated
leg: R posterior tibial, dorsalis pedis and L posterior tibial, dorsalis pedis
brachia: R and L arm
26
health promotion and maintenance of HTN
- weight reduction (through diet and exercise)
- DASH diet: dietary approach to stop hypertension (veggies, fruits, proteins, micronutrients, limited Na)
- reduce intake of dietary intake
- increase physical activity
- smoking cessation: nicotine causes vasoconstriction of blood vessels which increases BP
27
HTN diagnostic assessments
assess for secondary cause, risk and target organ damage
- urinalysis for protein, RBC (r/t kidney d/o, blood vessel constriction)
- Labs- BUN, creatinine
- chest x-ray (cardiomegaly: enlarged heart- mostly w people who have had HTN for a while)
- ECG shows degree of cardiac involvement
28
HTN patient problems (hint: think mngmnt and compliance)
- need for health teaching due to the plan of care for HTN management
- potential for decreased adherence due to side effects of drug therapy and necessary changes in lifestyle
29
HTN interventions: Lifestyle modifications
- Sodium restriction (2g Na diet)
- Weight reduction
- DASH diet (if overweight or obese)
- Moderation of alcohol intake (1-2/day if need it)
- Smoking cessation (cut back at least)
- Exercise (decrease weight and reduce vasoconstriction)
- Relaxation techniques (to help with stress)
- Caffeine avoidance (if applicable)
30
HTN interventions: drug therapy
First Line Options
- Diuretics: HCTZ, furosemide
- Calcium channel blockers:
Dihydropyridines: Amlodipine
Non-Dihydropyridines: Diltiazem/Verapamil
- ACE inhibitors: Lisinopril
- Angiotensin II receptor antagonists: Valsartan, Losartan
Secondary Options (may be paired with 1st line)
- Beta-blockers: Metoprolol
- Central alpha agonists: Clonidine
31
diuretic water slide
thiazide, loop, and potassium-sparing
- work on kidneys; increase UO to decrease BP
- take in morning (enuresis)
- stay hydrated- don't want to become dehydrated
- check BP before and after med
- monitor electrolytes daily: potassium (hypokalemia) (spironolactone- hyperkalemia)
- daily weights
- I&Os are equal (daily)
32
calcium channel blockers: action
blocks calcium access to cells
- decrease contractility
- decreased conductivity of the heart
therefore reducing demand for O2
33
side effects of calcium channel blockers
- decreased BP
- bradycardia
- may precipitate A-V block
- HA
- abdominal discomfort (constipation, nausea)
- peripheral edema
34
angiotensin II receptor blockers (ARBs): action
decrease blood pressure
- treat HTN and heart failure
- taken PO
35
angiotensin II receptor blockers (ARBs): drugs
usually end in "-sartan"
- candesartin
- valsartin
- irbestartan
- losartan
36
ACE inhibitors: name ends in
ends in "pril"
- lisinopril
- enalapril
- benzapril
- captopril
37
ACE inhibitors: action
decreases peripheral vascular resistance WITHOUT
- increased cardiac output
- increased cardiac rate
- increased cardiac contractility
38
ACE inhibitors: side effects
- dizziness
- orthostatic hypotension
- GI distress
- nonproductive cough***
- HA
- electrolytes: hyperkalemia
39
B-blockers ends in
"olol"
- metoprolol
- atenolol
- propranolol
40
B-blockers: action
blocks beta receptors in the heart causing:
- decreased heart rate
- decreased force of contraction
- decreased rate of AV conduction
**check BP and HR before giving med
41
B-blockers: side effects
- bradycardia
- GI disturbance
- CHF
- decreased BP
- depression
42
drug-nutrient interactions with calcium channel blockers (CCBs)
The grapefruit conundrum- Calcium channel blockers
- interferes with absorption causing higher drug level results
- GI complaints (constipation, nausea)
- Headache
- Flushing
- Bradycardia or reflex tachycardia
- Skin rash
43
principles of nutrition therapy for HTN patients
- Weight management: Lose weight and maintain appropriate weight for height
- Sodium control (2 g/day maximum)
- Other minerals: calcium, potassium, magnesium
- DASH diet: Lower blood pressure through diet alone
- Additional lifestyle factors: smoking, alcohol, caffeine, exercise
44
self-management education
- Teach medication compliance, usually for the rest of life
- Discuss goals of therapy, potential side effects, and how to identify potential problems
- Assist patient to understand therapeutic regimen
- Discuss consequence of noncompliance: organ failure: kidney failure (dialysis), heart: MI, brain: CVA
45
emergency care for HTN crisis (interventions)
- Place pt in semi-fowler's
- Administer O2
- Administer IV nitroprusside: dilates blood vessels and reduces BP
- Monitor BP q5-15 mins: want BP to come down gradually over a few hours (need to go to ICU for this degree of monitoring/care*)
- Observe for neurologic or cardiovascular complications (LOC; s/ CVA: weakness, speech, facial drooping; MI)
46
HTN crisis s/sx
- Extremely high BP
- Dizziness
- Blurred vision
- Disoriented
- Severe HA
47
HTN outcomes
- Verbalize understanding of the plan of care, including drug therapy and any necessary lifestyle changes
- Report adverse drug effects, such as coughing, dizziness, or sexual dysfunction, to the primary health care provider immediately
- Consistently adhere to the plan of care, including regular follow-up with the primary health care provider
48
peripheral vascular disease
- Disorders that alter the natural flow of blood through the arteries and veins of the peripheral circulation
- Divided into PAD and PVD
49
PAD is the result of
systemic atherosclerosis
50
PVD risk factors
- Advancing age
- obesity
- HTN
- DM
- +smoker
- hyperlipidemia
- African American
51
PAD
Disorders that alter the natural flow of blood through the arteries and veins of the peripheral circulation
- PVD implies arterial disease
52
PVD: physical assessment
Intermittent claudication
Pain that occurs even while at rest; numbness and burning
Inflow disease
- Discomfort in lower back, buttocks, thighs
Outflow disease
- Burning or cramping in calves, ankles, feet, toes
53
six P's of arterial insufficiency
- Pain
- Pallor
- Pulselessness (use doppler if can't feel to confirm no pulse)
- Paresthesia
- Paralysis: cant feel feet or legs
- Poikilothermia (coolness of extremities), numbness, tingling
54
PAD physical assessment (integumentary findings)
Hair loss and dry, scaly, pale or mottled skin and thickened toenails
55
severe arterial disease physical assessment
extremity is cold and gray-blue or darkened; pallor may occur with extremity elevation; dependent rubor; and/or muscle atrophy
56
PVD dx assessment
Imaging assessment
- Arteriography: contrast dye used to see blood vessels; most invasive- iodine allergy risk
Other diagnostic tests:
- Ankle-brachial index (ABI)** (blood pressure in arms/legs, <0.9=PAD)
- Exercise tolerance testing: treadmill and heart monitor- how far before claudication
- Plethysmography: graph of BP readings
57
PVD non-surg interventions
Exercise (walking as tolerated)
Positioning (controversial)
Promoting vasodilation
Drug therapy (Antiplatelet agents-ASA, Clopidogrel)
Control HTN
58
PVD surg interventions
Arterial revascularization
59
PVD: invasive non-surgical
Percutaneous transluminal angioplasty (stents)
Laser-assisted angioplasty (smaller occlusions)
Atherectomy
60
clopidogrel (plavix)
antiplatelet medication
- prevents PVD/PAD
- watch skin and URI as s/e
- caution with HTN, renal/hepatic problems, hx of bleeding
61
PVD surgical management
aortoiliac and aortofemoral bypass surgery
62
aortoiliac and aortofemoral bypass: procedure
a midline incision into the abdominal cavity is required, with an additional incision in each groin
63
Postoperative care after aortoiliac and aortofemoral bypass
Deep breathing every 1 to 2 hour
Monitor for graft occlusion (emergency)
Treatment of graft occlusion
Monitor for compartment syndrome
Assess for infection
Assess GI function
64
PAD discharge teaching
Keep feet clean and dry (check between toes)
Always wear shoes and make sure fit right
Keep toenails clean and filed (Podiatrist)
Apply lubricating lotion to feet if dry
Prevent exposure to extreme heat or cold
Avoid constricting garments
See Podiatrist or HCP if problem develops
Avoid extended pressure on feet or ankles
65
acute peripheral arterial occlusion
Embolus—the most common cause of occlusions, although local thrombus may be the cause
- sudden and dramatic
- more common in lower extremities
66
acute peripheral arterial occlusion: assessment
six P's
pain, pallor, pulselessness, paresthesia, paralysis, poikilothermia (coolness)
67
acute peripheral arterial occlusion drug therapy
anticoagulant drug therapy with unfractioned heparin (UFH) is first intervention to prevent further clot formation
68
acute peripheral arterial occlusion surgical therapy
Thrombectomy or embolectomy: removes occlusion (clott)
arteriotomy: surgical opening of artery to retrieve embolus
69
acute peripheral arterial occlusion nursing care
- Monitor for compartment syndrome
- prompt treatment
- monitor for spasms, swelling of skeletal muscles (compartment syndrome)
70
acute peripheral arterial occlusion interventions
- Prompt treatment is important to prevent permanent damage or loss of extremity
- Thrombectomy or embolectomy
- Monitor for compartment syndrome
71
aneurysm
a permanent localized dilation of an artery, enlarging the artery to twice its normal diameter
- worried about it rupturing
71
aneurysms of central arteries
Fusiform aneurysm (affects entire circumference)
Saccular aneurysm (out-pouching of part of wall)
Dissecting aneurysm (aortic dissection)
- Blood accumulates in the wall of artery
72
Abdominal aortic aneurysm
aneurysm in an abdominal artery
- common
73
Thoracic aortic aneurysm
aneurysm in a thoracic artery
- not as common as abdominal
74
arterial aneurysms
aneurysm in the artery
75
Aneurysms of Central Arteries
are sometimes (hint: sx)
- sometimes asymptomatic
76
TAA: thoracic aortic aneurysm (assessment: s/sx)
- Back pain
- Shortness of breath
- Difficulty swallowing
- Not often detected by physical assessment
- May have a mass above the suprasternal notch
77
AAA: abdominal aortic aneurysm (assessment)
- Gnawing pain with abdominal, flank, or back pain
- Pulsation in upper abdomen
- Detectable = at least 5 cm in diameter
- Rupture symptoms = severe sudden pain in back, low abdomen; radiates to groin, buttocks, legs
- Critical illness – at risk for hypovolemic shock caused by hemorrhage
78
aneurysms dx assessment
- Abdominal or lateral XR of spine shows AAA with “eggshell” appearance.
- *CT: gold standard for assessing size and location of abdominal or thoracic aneurysm. (best test for dx and monitoring)
- Thoracic aneurysm can be diagnosed by CXR.
- Aortic arteriography used in patients prior to repair of thoracic aneurysm.
- Ultrasonography used to diagnose, locate, and measure size of aneurysm.
79
aneurysms nonsurgical management
- Monitor the growth of the aneurysm (w/ CT scans)
- Maintain BP at a normal level to decrease the risk of rupture
- Treat HTN with anti-hypertensive drugs
- Frequent CT scans for small or asymptomatic aneurysms
80
aneurysms patient teaching
importance of keeping every appointment
going for scheduled tests
clinical manifestations that need to be reported promptly
81
endovascular stent grafts
*Procedure of choice for almost all AAA repairs
- Decreased morbidity and mortality and shorter length of stay compared to surgical resection
- Graft placed percutaneously: small insertion going into femoral vein threaded into the abdominal or arterial aorta
- Closely monitor for complications
82
endovascular stent grafts complications
- Conversion to open surgical repair
- Bleeding
- Rupture
- Peripheral embolization
- Misplacement of graft
- Endoleak: need this repaired in OR
- Infection
82
signs of graft occlusion or rupture
- Changes in (peripheral) pulses
- Cool to cold extremities below the graft
- White or blue extremities or flanks
- Severe pain
- Abdominal distention
- Decreased urine output
83
Thoracic Aortic Aneurysm Repair pre-op care
same as abdominal
84
Thoracic Aortic Aneurysm Repair operative procedure
same as abdominal
- endovascular stent graft
85
Thoracic Aortic Aneurysm Repair post-op care assessments
- Vital signs
- Complications
- Sensation and motion in extremities: distal pulses, color, temp
86
Thoracic Aortic Aneurysm Repair post-op complications
Hemorrhage
Ischemic colitis
Cerebral or spinal cord ischemia
Respiratory distress: RR, pulse ox
Infection
Cardiac dysrhythmias: irreg heartbeat
87
d/c instructions post aneurysm repair
- activity restrictions: cant drive for a few weeks, limit stair climbing (1-2x/day limit) for a few weeks, no heavy lifting (<15 lb) for a few weeks
- wound care: infection, bleeding, inspect redness, swelling, edema- call HCP
- pain management: acetaminophen (don't use NSAIDs/ibuprofen bc increases bleeding)
88
aortic dissection
sudden tear in the aortic intima, opening the way for blood to enter the aortic wall
89
aortic dissection assessment findings
Pain described as tearing, ripping, and stabbing
Diaphoresis, N/V, and feeling faint
BP usually WNL
↓ or absence of peripheral pulses
Aortic regurgitation
Altered LOC
Paraparesis (lower extremity weakness)
Stroke
90
aortic dissections dx labs
CXR, CT, MRI or aortic angiography
TEE at bedside for patients that can’t be moved
91
aortic dissection emergency care goals
Elimination of pain
Reduction of blood pressure (IV Nipride)
Decrease in the velocity of left ventricular ejection
92
aortic dissection surgical treatment
proximal dissection; typically requires cardiopulmonary bypass (CPB)
- surgeon removed the intimal tear and sutures edges of the dissected aorta
- synthetic graft used usually
93
aortic dissection nonsurg treatment
- BP maintenance: CCAs calcium channel agonsists, BBs beta blockers
- large bore IV catheters infusing 0.9% NaCl and give medication
- pain control and IV BB: to decrease HR and BP
- nitroprusside or nicardipine hydrochloride may be used if pain control IV BB doesnt work
94
Aneurysms of the Peripheral Arteries
- femoral
- popliteal
95
Aneurysms of the Peripheral Arteries sx
limb ischemia
diminished or absent pulses
cool to cold skin
pain
96
Aneurysms of the Peripheral Arteries: you should not do what
- DO NOT PALPATE TO PREVENT RUPTURE
97
Aneurysms of the Peripheral Arteries post-op care
monitor for pain
ischemia
98
raynaud's phenomenon
Caused by vasospasm of arterioles and arteries of upper and lower extremities
99
raynaud's phenomenon drug therapy
Calcium channel blockers
100
raynaud's phenomenon interventions
Restrict cold exposure
Avoid vasoconstrictors
Avoid Caffeine
Stop smoking
Reinforce patient education
Lumbar sympathectomy
*lifestyle changes and drug therapy (CCB)
101
venous disorders sx
- will feel pedal pulses
- warm
- legs
- blood is getting down but can't get back up
102
VTE
Thrombus—a blood clot
Virchow’s triad
Thrombophlebitis
Pulmonary embolism
Phlebitis (vein inflammation)
103
risk assessment for VTE
Assesses risk and not to diagnose
Points for each risk factor
Consider Virchow's Triad
- Blood flow stasis: long plane/car ride/immobility
- Endothelial injury: higher risk
- Hypercoaguability: cancer, thrombophilia, blood clotting d/o
104
interventions to prevent VTE: outpatient
Avoid oral contraceptives
Drink adequate fluids to avoid dehydration
Exercise legs during long periods of BR or sitting
105
interventions to prevent VTE: inpatient
Patient education
Leg exercises
Early ambulation
Adequate hydration
Graduated compression stockings
Anticoagulants for high risk
106
assessment for VTE
*Calf or groin tenderness or pain
*Sudden onset of unilateral swelling of the leg
*NO Homans’ sign
*Induration
*Localized edema
*Venous duplex ultrasonography
MRI
D-dimer: may be elevated
107
Nonsurgical Management VTE
- Rest – no risk of PE with ambulation (dont want clot to dislodge/move)
- Drug therapy includes:
- Unfractionated IV heparin therapy
- Low–molecular weight heparin (anoxaparin)
- Warfarin therapy
- Direct Oral Anticoagulants (DOAC) (apixaban: eliquis)
- Thrombolytic therapy
- Do not message extremity to avoid dislodgement (to brain causing stroke)
108
Anticoagulants
used for prophylaxis and treatment of thromboembolic disorders like DVT, PE
- heparin
- warfarin
109
heparin
- Potentiates the inhibitory effect of antithrombin on factor Xa and thrombin
- *IV or SQ route
- ***Monitor aPTT (parameters based off hospital policies)
- Therapeutic level 1.5 -2.5 times control (50-70/ 0.3-0.7 control)
- Monitor for bleeding
- Protamine sulfate
110
warfarin
- Interferes with vitamin K-dependent clotting factors (II, VII, IX, and X)
- *PO
- ***Monitor INR (parameters based off hospital policies)
- Therapeutic level 2-4.5 times control (2-3/0.8-1.1 control)
- Monitor for bleeding
- Vitamin K
- takes 3-4 days to work, take heparin and warfarin until INR is therapeutic
111
low molecular weight heparin: Enoxaparin
Low molecular weight
Orthopedic surgeries
dVt prophylaxis, immobility, stints, cardiac surgeries - indicators
lEave bubble in syringe
Never by IM, only SQ- give within 2 hours of preop abdominal surgery and 12 hours at knee surgery
nO rubbing after admin, no aspiration, no mixing with other drugs
X out for pork allergies, heparin allergies, PUD, leukemia
"love an ox" by initiating bleeding protocols, having protamine sulfate on hand for antidote and monitoring coag studies
112
Nursing Interventions for Patients Receiving Anticoagulants
Check dosage of drug
Monitor VS
Vitamin K or protamine sulfate on hand
Monitor aPTT for IV heparin; INR for warfarin
No monitoring for DOAC
Apply prolonged pressure over venipuncture and injection sites
Apply pressure, no massage, when giving SQ heparin
113
Teaching for Patients Taking Anticoagulants
Stop smoking
Stop BCPs
Use electric razor
Soft toothbrush
Precautions to avoid injury (no hammers/ saws)
Report signs/symptoms of bleeding to HCP
Take prescribed dosage of drug at ordered time
Do not stop taking drug unless instructed by HCP
Avoid foods/drugs that can interfere with warfarin: no leafy greens, broccoli, brussels sprouts, liver, ASA, tylenol, laxatives/antacids, ABT
Keep appointments for blood draws
114
surgical management of VTE
- Thrombectomy: removes blood clotts in an artery or vein to restore blood flow through the blood vessel
- Inferior vena caval interruption (IVC filter)
- postop monitoring: for bleeding at incision site (groin), skin color, temperature, peripheral pulses, sx of infections
115
stage 1 HTN according to JNC-8
SBP: 140-159
DBP: 90-99
*at least two elevated readings in both arms on separate occasions to dx
116
stage 2 HTN according to JNC-8
SBP: > 160
DBP: > 100
*at least two elevated readings in both arms on separate occasions to dx
117
HTN assessment
- history: family hx, PMH, current/past diagnoses
- physical assessment: often asymptomatic, blurry vision, dizziness, hA
- psychological assessment: stressed? job? marital life? sick family member?
- dx assessment: readings from taking BP, debate primary v secondary
118
potassium-rich foods for patients taking diuretics
- bananas
- citrus (orange, cantaloupe, orange juice)
- leafy greens
119
diuretics side effects
- decrease K
- decrease Na
- decrease Cl
- decrease BP
- decrease I&Os
- decrease weight
- hyperglycemia
- dehydration
120
what causes a HTN crisis?
usually med noncompliance
- abrupt discontinuance of HTN medications
121
arteriosclerosis
hardening/thickening of the arterial wall
- arteries thicken, no flexible/no elasticity
- associated with aging
122
atherosclerosis
result of fatty plaque build up
- type of arteriosclerosis
- formation of plaque within the arterial wall
- leading cause of CVD
123
inflow obstructions
blockage iliac and up
- discomfort in lower back, buttocks, thighs
124
outflow obstructions
blockage femoral and down
- burning or cramping in calves, ankles, feet, toes
125
PAD physical assessment: stage 1
- no claudication
- may hear bruit
- pedal pulses decreased or absent
126
PAD physical assessment: stage 2
- intermittent claudication with exercise
127
PAD physical assessment: stage 3
- rest pain, awakens at night
- numbness and burning
- pain in toes, arch, heel
- pain relieved by placing extremity in dependent position
128
PAD physical assessment: stage 4
- ulcers and blacked tissue occur on toes, forefoot, and heel (necrosis)
- gangrenous odor
129
Preoperative care before aortoiliac and aortofemoral bypass
- document VS and peripheral pulses
- IV antibiotic before surgery
130
padua prediction score
assessment tool to assess for VTE, not to diagnose
- points for each risk factor
- score >4 means VTE more likely
NU 340
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