1
Q
Peripheral Artery Diseases
A
- Critical limb ischemia
- Acute arterial ischemic disorders
- Aneurysms of the central arteries
- Aortic dissection
2
Q
Causes for impaired delivery of oxygenated blood?
A
- Artherosclerosis, emboli
- Sluggish flow or blood loss
3
Q
Consequences of Ischemia
A
- Tissue death: ulcers, non-healing wounds
- Organ/limb dysfunction
- Pain
- Possible low BP
- Death
4
Q
What structures does atherosclerosis involve?
A
- Aorta
- Lower extremity arteries
5
Q
What can atherosclerosis cause?
A
- Aneurysm due to weak, buldging arterial wall
- Risk for rupture
6
Q
How does PAD present?
A
- Intermittent claudication (pain with walking)
- Critical limb ischemia
- Acute arterial ischemia
7
Q
What happens in PAD?
A
Narrowing + hardening of blood vessels causing the restriction of blood flown to preipherals
8
Q
What populations are most impacted by PAD?
A
Adults over 50
Those with CAD
9
Q
Risk factors for PAD?
A
HTN
Smoking
DM
CAD
10
Q
Most common places for PAD in DM2?
A
Below knee
Tibial and Peroneal arteries
Smaller arteries are harder to treat
11
Q
Most common places for PAD in those WITHOUT DM2?
A
Above knee
Femoral Artery
Popliteal
Larger arteries are easier to treat
12
Q
Lower leg appearence with PAD
A
- Pale
- Hairless
should be bilat
13
Q
Lowe Leg temp with PAD
A
Cool
14
Q
Peripheral pulses with PAD
A
Dimished
Absent
15
Q
Nails with PAD
A
- Thickened
- Brittle
- Yellow
16
Q
Skin colour in PAD
A
- Dependent rubor
- Elevated pallor
17
Q
PAD ulcers
A
- Punched out, defined circles
- Drainage is minimal
- Pale, Pale pink in colour
18
Q
Best way to maximize blood flow to feet with PAD
A
Gravity
19
Q
6 P’s of PAD
A
- Pallor
- Pain
- Paresthesia
- Paralysis
- Poikilothermia
- Pulselessness
20
Q
PAD Dx
A
- Ankle-Brachial index
- Computed tomographic angiography
- Angiography (invasive) Angiogram
- Doppler ultrasound studies
- Duplex imaging
21
Q
PAD management
A
- Lifestyle changes
- Medications
- Complementary & alternative therapies
- Surgery (Vascular)
- Potential amputation
22
Q
Collateral Circulation in PAD
A
- Natural bypass vessels may develop
- Often inadequate in advanced disease
23
Q
Critical limb ischemia
A
- Rest pain >2 Weeks
- Non-healing ulcers
- Gangrene
- Common in pts with DM, HF, Prior stroke
24
Q
Intermittent Claudication
A
- Reproducible pain with exercise relieved by rest
- Due to anaerobic metabolism and lactic acid build up
25
What determines pain location in PAD?
Blockage site
26
Buttock/Thigh pain blockage site
Aortoiliac
27
Calf pain blockage site
Femoral or popliteal
28
Foot pain blockage site
Tibial or peroneal
29
Why is PAD so painful?
- Blood flow can't meet oxygen demands of working muscle
- In advanced stages, even rest doesn't restore perfusion
30
PAD treatments
- Exercise therapy
- Managing risk factors
- Medications
- Revascularization
- Wound care
- Amputation
31
What are interventions used for restoring blood flow in PAD?
- Interventional radiological Catheter-Based Procedures
- Surgical Interventions
| If an artery is occluded, goal is to restore blood flow (revascularize)
32
What are some examples of Interventional Radiological Catheter-Based Procedures?
Percutaneous transluminal angioplasty
- stents are placed in
Atherectromy
- Removes plaque from artery
33
What are some examples of surgical interventions for PAD?
Peripheral artery bypass surgery
- Uses either autogenous vein or graft
Endarterectomy
- Removes plaque from vessels
Patch Graft Angioplasty
- Prevents plaque from dislodging
Amputation
- Last resort
34
What is the standard for post-op checks for a pt with PAD?
q15 for 4 checks = 1hr
q30 for 4 checks = 2hr
q60 for 4 checks = 4hr
If CWSM good then q4hr checks
35
What does image A depict?
Fem-pop Bypass
- fem-pop bypass graft around occluded superficial femoral artery
36
What does image B depict?
Femoral-posterior tibial bypass graft around occluded superficial femoral, popliteal and proximal tibial arteries
37
PAD post op care monitoring
- Vs (q15, q30, q60 etc)
- CWSM
- Cap refill
- Pulses/doppler
- report decreased or absent pulses/doppler changes
- ABI should increase from baseline and stay stable
38
PAD post-op pain and complications
- Chronic ischemia may increase opioid tolerance, pain team may be needed
- Watch for bleeding **increased pain, decreased pulses or ABI, pallor, numbness, cyanosis**
- Hypotension = graft failure risk
39
PAD post-op mobility and positioning
- Avoid knee flexion
- Reposition often; avoid prolonged leg dependency
- Elevate edematous limb above heart
- Walk with support
40
PAD post-op wound care and discharge
- Monitor for SSI, may need adbanced care
- Discharge if stable: typically 3-5 days
41
What is the aorta?
Largest artery, supplying oxygenated blood to all vital organs
42
What is an aortic aneurysm?
**Localized dialation of the aorta** either **Congenital** or **Acquired**
43
Abdominal aortic aneurysms (AAA)
- 75% of AA
- most commonly infraneal (below renal arteries)
44
Thoracic aortic aneurysms (TAA)
25%
- Other less common sites include: popliteal, illiac, femoral
45
Risk factors for aneurysms
- >65 yo
- **Males
- Smoking
- Atherosclerosis
- HTN
- Family Hx**
- CT disorders (Marfans, ED)
46
What is a true aneurysm?
- Involves all three layers of the arterial wall
- Fusiform (identical on both sides)
- Saccular (more buldgey on one side)
47
What is a false aneurysm?
Pseudoaneurysm
- Disruptipn of vessel wall
- Contained by surrounding tissue
48
CM of AAA
- Often asymptomatic
- May feel **pulsatile abd mass**
- Back/epigastric pain
- Bruit
49
CM of TAA
- sharp, stabbing chest/back pain
- Dysphagia
- JVD
- Edema
50
AAA complications
**Rupture**
- life threatening
- presents as severe pain, hypotension, shock symptoms, Greys Turners sign
51
Rupture mortality rate?
40% of ruptures are lethal within minutes
60% left untreated are lethal within 48hrs
52
Surgical interventions for AAA
- Open aneurysm repair
Very invasive
- Endovascular intervention repair time
Minimally invasive
53
What is required before open surgical repair of an aneurysm?
The patient must be hydrated, and any electrolyte, coagulation, and hematocrit abnormalities must be corrected.
54
What is the mortality rate for ruptured AAAs?
The mortality rate can be as high as 90%.
55
What effect does screening have on ruptured AAAs?
Screening has been shown to lower the death rate.
56
What are the steps involved in open aneurysm repair?
1. Incise the diseased aortic segment. 2. Remove any thrombus or plaque. 3. Suture a synthetic graft to the aorta proximal and distal to the aneurysm. 4. Suture the native aortic wall around the graft.
57
What is done if the iliac arteries are also aneurysmal?
A bifurcated graft replaces the entire diseased segment.
58
How can saccular aneurysms be repaired?
It may be possible to excise only the bulbous lesion and repair the artery by primary closure or by application of a patch graft.
59
What is autotransfusion in AAA surgery?
Autotransfusion recycles the patient’s own blood to reduce the need for blood transfusions.
60
What is necessary during AAA resections?
Aortic cross-clamping proximal and distal to the aneurysm is necessary.
61
What is cross clamping?
Cross clamping proximal and distal to aneurysm
62
What is cross-clamp time
In open procedure top + bottom is clammped, it is critical to know this time perserve perfusion
63
How long do most resections take?
Most resections are performed in 30 to 45 minutes.
64
What should be ensured before closing the abdominal incision?
Adequate renal perfusion after clamp removal should be ensured if the cross-clamp is applied above the renal arteries.
65
What is the risk of postoperative renal complications?
The risk increases significantly when surgical repair of AAAs is above the level of the renal arteries.
66
What complications may arise if the clamp is supraceliac?
The risk of postoperative bowel complications, such as ischemic bowel, increases and should be monitored closely.
67
What is endovascular aneurysm repair (EVAR)?
Minimally invasive procedure that includes aortic, thoracic, and fenestrated grafts. It is an alternative to open aneurysm repair.
68
What are the components of endovascular approaches?
Placement of a sutureless aortic graft into the abdominal aorta via the femoral artery.
69
What materials are used in grafts for EVAR?
Grafts can be made of various materials, such as a Dacron cylinder supported with flexible wire.
70
How is the graft delivered during EVAR?
The main section of the graft is bifurcated and delivered through a femoral artery catheter.
71
What happens after all graft components are in place?
They are deployed against the vessel wall by balloon inflation, creating a circumferential seal.
72
What is the outcome of blood flow through the endovascular graft?
It prevents further expansion of the aneurysm and allows the aneurysmal wall to shrink over time.
73
What are the advantages of EVAR over open aneurysm repair?
EVAR is less invasive, requires a shorter hospital stay, and has fewer complications.
74
What is the most common complication of AAA repair?
Endoleak, which is the seepage of blood back into the old aneurysm.
75
What complications can arise from endovascular repair?
Aneurysm growth, rupture, aortic dissection, bleeding, renal artery occlusion, graft thrombosis, hematoma, and infection.
76
What is intra-abdominal hypertension (IAH)?
A potentially lethal complication that reduces blood flow to the viscera during emergency repair of a ruptured AAA.
77
How is IAH confirmed?
By measuring the patient’s intra-abdominal pressure indirectly through a catheter and transducer system.
78
What are the treatment goals for IAH?
Control of situations that lead to IAH, including surgical decompression and conservative measures.
79
What does EVAR include?
Aortic, Thoracic and fenestrated
80
Pre-op care for aneurysm repair
- Assess cardio, neuro, renal and pulmonary status
- Educate on procedures, mark pedal pulses, monitor for rupture signs
81
Post-op care for aneurysm repair
- VS
- urine output
- Neuro checks
- Graft perfusion
82
Post op risks for aneurysm repair?
Watch for signs of infection
paralytic illeus if BS not present for more then a few hours
Renal failure (monitor creatin and urine output)
83
Pain control and emotional support for aneurysm repair
PCA/epidural
Education for patients and family
84
85
What is aortic dissection?
Aortic dissection is a tearing of the inner layer of the vessel that results in the creation of a false lumen through which blood flows.
86
What are the goals for aortic dissesction care?
Prevent rupture
Managed S&S
87
How is aortic dissection classified?
Aortic dissection is classified based on anatomical location (ascending versus descending aorta) and duration of onset (acute versus chronic).
88
What is Type A dissection?
Type A dissection affects the ascending aorta and arch, requiring emergency surgery.
89
What is Type B dissection?
Type B dissection begins in the descending aorta, allowing for potential conservative management.
90
What are the time classifications for aortic dissection?
Dissections are classified as acute (first 14 days), subacute (14 to 90 days), or chronic (greater than 90 days) based on symptom onset.
91
What causes nontraumatic aortic dissection?
Nontraumatic aortic dissection is caused by weakened elastic fibres in the arterial wall, often accelerated by chronic hypertension.
92
What is believed to initiate aortic dissection?
Aortic dissection is believed to arise from an intimal tear, typically occurring in areas with the greatest rate of rise of blood pressure.
93
What are the risk factors for aortic dissection?
Risk factors include hypertension, age, aortic diseases, atherosclerosis, blunt trauma, tobacco use, drug use, congenital heart disease, connective tissue disorders, family history, history of heart surgery, and pregnancy.
94
What are common clinical manifestations of acute type A aortic dissection?
About 80% of patients report an abrupt onset of severe anterior chest or back pain.
95
How does pain presentation differ between type A and type B dissections?
Patients with acute type B dissection are more likely to report pain in their back, abdomen, or legs.
96
What symptoms may indicate involvement of the aortic arch?
Neurological deficits such as altered level of consciousness, weakened or absent carotid and temporal pulses, and dizziness or syncope may occur.
97
What is a severe complication of acute ascending aortic dissection?
Cardiac tamponade, which occurs when blood leaks into the pericardial sac, is a severe complication.
98
What are the clinical manifestations of cardiac tamponade?
Clinical manifestations include hypotension, narrowed pulse pressure, jugular venous distension, muffled heart sounds, and pulsus paradoxus.
99
What diagnostic studies are used for aortic dissection?
Diagnostic studies include chest radiograph, three-dimensional CT scanning, MRI, and transesophageal echocardiography.
100
What does a chest radiograph show in aortic dissection?
A chest radiograph may show a widening of the mediastinum and pleural effusion.
101
What is preferred in unstable patients for diagnosing aortic dissection?
Transesophageal echocardiography is preferred in very unstable patients or those with contraindications to CT or MRI.
102
What are the different ypes of peripheral venous disease?
- Venous Thromboembolism
- Venous ulcers
-Venous insufficiency
103
What is DVT prophylaxis?
DVT prophylaxis refers to the measures taken to prevent Deep Vein Thrombosis (DVT).
## Footnote
Prevention is different than treatment.
104
What are some active exercises for DVT prevention?
Active exercises include position changes, getting out of bed, and walking.
105
What are TED stockings and SCDs?
TED stockings and Sequential Compression Devices (SCDs) are used to promote blood flow and prevent DVT.
106
What types of anticoagulation are used for DVT prevention?
Anticoagulation options include heparin subcutaneously, LMWH subcutaneously, and Apixaban orally.
107
What is the first line of treatment for confirmed DVT?
Anticoagulant therapy.
108
What anticoagulants are used in DVT treatment?
Heparin continuous infusion and warfarin po.
| Heparin is used until therapuetic INR
109
How is Heparin dosage adjusted?
Heparin dose adjustment is based on PTT value; antidote is Protamine Sulfate.
110
How is Warfarin dosage adjusted?
Warfarin dose adjustment is based on INR value; antidote is Vitamin K.
111
What assessments are necessary for DVT patients?
Regular assessments including vital signs and signs of complications.
112
What type of oxygen source should be provided?
Humidified O2 source.
113
What aspects of care should be monitored in DVT patients?
Nutrition and hydration.
114
What signs and symptoms should be recognized in DVT patients?
Signs and symptoms of pulmonary embolism (PE).
115
What is venous thromboembolism (VTE)?
VTE, also known as venous thrombosis, is a condition in which a thrombus forms in association with inflammation of the vein.
116
What are the two classifications of venous thromboembolism?
VTE is classified as either superficial vein thrombosis (SVT) or deep vein thrombosis (DVT).
117
What is superficial vein thrombosis (SVT)?
SVT is the formation of a thrombus in a superficial vein, usually the greater or lesser saphenous vein.
118
What is deep vein thrombosis (DVT)?
DVT is a disorder involving a thrombus in a deep vein, most commonly the iliac and femoral veins.
119
What is the risk associated with superficial vein thrombosis (SVT)?
Patients with SVT are at risk for VTE and need workup including a vascular lab if any risk factors exist.
120
What are the three factors that cause venous thrombosis?
The three factors are (a) venous stasis, (b) damage of the endothelium, and (c) hypercoagulability of the blood.
121
What causes venous stasis?
Venous stasis occurs when the valves are dysfunctional or the muscles of the extremities are inactive.
122
Who is more likely to experience venous stasis?
Venous stasis occurs more often in people who are obese or pregnant, have chronic heart failure, or have been immobile for long periods.
123
What can cause endothelial damage?
Endothelial damage may be caused by direct injury (e.g., surgery, trauma) or indirect injury (e.g., chemotherapy, sepsis).
124
What is hypercoagulability of blood?
Hypercoagulability occurs in many hematological disorders and can be caused by certain medications, including corticosteroids and estrogens.
125
Who is at increased risk for VTE?
Women of childbearing age who take estrogen-based oral contraceptives or who are pregnant are at increased risk for VTE.
126
How does smoking affect the risk of thrombus formation?
Smoking causes hypercoagulability by increasing plasma fibrinogen and homocysteine levels and activating the intrinsic coagulation pathway.
127
What are important past health history factors for venous thromboembolism?
Trauma to vein, intravascular catheter, varicose veins, pregnancy or recent childbirth, bacteremia, obesity, prolonged bed rest, irregular heartbeat, COPD, HF, cancer, coagulation disorders, systemic lupus erythematosus, MI, spinal cord injury, stroke, prolonged air travel, recent bone fracture, dehydration.
128
What medications are associated with venous thromboembolism risk?
Use of estrogens, tamoxifen, corticosteroids, excessive amounts of vitamin E, IV use of illicit drugs.
129
What surgeries or treatments increase venous thromboembolism risk?
Any recent surgery (especially orthopedic, gynecological, gastric, or urological), previous surgery involving veins, central venous catheter.
130
What symptoms may indicate venous thromboembolism?
Pain in area on palpation or ambulation.
131
What general objective data may be observed in venous thromboembolism?
Fever, anxiety, pain.
132
What integumentary signs may indicate venous thromboembolism?
Increased size of affected extremity, taut, shiny, warm skin, erythematous skin, tenderness to palpation. Some patients may have no physical changes.
133
What cardiovascular signs may indicate venous thromboembolism?
Distension and warmth of superficial veins, edema and cyanosis of extremities, neck, back, and face (if superior vena cava involvement).
134
What are possible laboratory findings in venous thromboembolism?
Leukocytosis, abnormal coagulation, anemia or increased hematocrit and RBC count, increased D-dimer level, positive venous compression on duplex ultrasound, positive findings on CTV, magnetic resonance venography, or contrast venography.
135
What laboratory tests should be evaluated for patients receiving anticoagulants?
Evaluating appropriate laboratory coagulation tests for target therapeutic levels, if appropriate.
136
What should be assessed in the lower extremities of patients using intermittent compression devices?
Evaluating lower extremity for ecchymosis/hematoma development.
137
What is important to monitor regarding platelet count in patients on anticoagulants?
Evaluating platelet count for signs of heparin-induced thrombocytopenia (HIT).
138
What signs should be examined in urine and stool for patients on anticoagulants?
Examining urine and stool for overt signs of blood.
139
What skin assessments should be performed on patients receiving anticoagulants?
Inspecting skin frequently, especially under any splinting devices.
140
What vital signs should be monitored in patients on anticoagulants?
Monitoring vital signs as indicated.
141
What should be done if abnormalities are found in assessments or vital signs?
Notifying the health care provider of any abnormalities in assessments, vital signs, or laboratory values.
142
What risk assessment should be performed for patients on anticoagulants?
Performing assessment of risk for falling per institutional policy and implementing safety measures as needed.
143
What symptoms should be observed frequently in patients receiving anticoagulants?
Performing assessments frequently to observe for signs and symptoms of bleeding (e.g., hypotension, tachycardia), clotting, or both.
144
What should be done at venipuncture sites after injection?
Applying manual pressure for at least 10min (or longer if needed) on venipuncture sites.
145
What type of injections should be avoided in patients on anticoagulants?
Avoiding intramuscular injections.
146
How can venipunctures be minimized?
Minimizing venipunctures.
147
What type of needles should be used for venipunctures?
Using small-gauge needles for venipunctures unless ordered that therapy necessitates use of a larger gauge.
148
What should be administered to patients to avoid hard stools?
Administering stool softeners to avoid hard stools and straining.
149
What devices should be applied as ordered for patients on anticoagulants?
Applying graduated compression stockings or sequential compression devices as ordered and with attention to proper size, application, and use.
150
What should be applied to the skin of patients receiving anticoagulants?
Applying moisturizing lotion to skin.
151
What should be avoided regarding established clots?
Avoiding removal or disruption of established clots.
152
What type of restraints should be used if necessary?
Avoiding restraints if possible; using only soft, padded restraints if needed.
153
What instruction should be given to patients regarding nose blowing?
Instructing patient not to forcefully blow nose.
154
What type of clothing should patients avoid?
Instructing patient to avoid restrictive clothing.
155
What type of razors should patients use?
Instructing patient to use electric razors, not straight razors.
156
What should patients use for oral care?
Instructing patient to use soft toothbrushes or foam swabs for oral care.
157
What type of tape application should be limited?
Limiting tape application; using paper tape as appropriate.
158
What should be done to tubes before insertion?
Lubricating tubes (e.g., suction catheter) adequately before insertion.
159
How should physical care be performed for patients on anticoagulants?
Performing physical care in a gentle manner.
160
How should patients be repositioned?
Repositioning patient carefully at regular intervals.
161
What supportive devices should be used as indicated?
Using support pads, mattresses, and therapeutic beds as indicated.
162
Greenfield filter
Inferior vena caval interuption technique with a stainless steel filter to prevent PE
As blood travels up the vena cava, clots are trapped in the filter
163
What is chronic venous insufficiency?
- Common disorder
- Leg valves fail to keep blood moving forward
- Results in ambulatory venous HTN
- Leg ulcers
164
Who is at risks for CVI?
- Women
- Elderly
165
What is the cornerstone for CVI treatment?
Compression is the cornerstone for CVI treatment, venous ulcer healing, and prevention of ulcer recurrence.
166
What are the options available for compression therapy?
A variety of options are available for compression therapy:
• custom-fitted graduated compression stockings
• short stretch bandages
• multilayer bandage systems, including a two-layer (Coban) and four-layer system (Profore)
167
What should be included in the teaching plan for a patient receiving anticoagulant therapy?
Reasons for and basic mechanism of action of anticoagulant therapy, anticipated therapy duration, and availability of reversal agents.
168
What is the recommended time to take anticoagulant medication?
At the same time each day, preferably in the afternoon or evening.
169
What is the need for follow-up with blood tests in anticoagulant therapy?
To assess the therapeutic effect of the medication and determine if dosage changes are required.
170
What are some adverse effects of anticoagulant therapy that require medical attention?
Any bleeding that does not stop after 10–15 minutes, blood in urine or stool, chest pain, shortness of breath, severe headaches, unusual bleeding, and weakness or dizziness.
171
What should patients avoid to prevent trauma or injury while on anticoagulant therapy?
Vigorous brushing of teeth, contact sports, in-line roller skating, and use of straight razors.
172
What medications should be avoided unless prescribed by a specialist?
All ASA products and nonsteroidal anti-inflammatory drugs (NSAIDs).
173
What is the guideline for alcohol intake while on anticoagulant therapy?
Limit to small to moderate amounts: 341 mL (12 oz) of beer, 118 mL (4 oz) of wine, or 30 mL (1 oz) of hard liquor per day.
174
What should patients wear to indicate their anticoagulant therapy?
A Medic Alert bracelet or necklace indicating the anticoagulant being taken.
175
What dietary changes should be avoided while on anticoagulant therapy?
Frequent changes in eating habits, especially dramatically increasing foods high in vitamin K, and avoiding supplemental vitamin K.
176
What should patients do before starting or stopping any medication or supplement?
Consult with their health care provider.
177
Who should be informed about a patient's anticoagulant therapy?
All health care providers, including dentists.
178
What is necessary regarding dosing for patients on anticoagulant therapy?
Correct dosing is essential, and supervision may be required for patients experiencing confusion or cognitive impairment.
179
What is the pathophysiology of venous ulcers?
Venous hypertension leads to fluid and RBC leakage, causing edema and inflammation.
180
What causes brownish skin discoloration in venous ulcers?
Hemosiderin causes brownish skin discoloration.
181
What are the clinical features of venous ulcers?
Ulcers are located above the medial malleolus and are painful, especially when legs are down.
182
What skin changes are associated with venous ulcers?
Brown skin discoloration, itching (stasis dermatitis), and edema are common.
183
What is the primary management for venous ulcers?
Compression therapy using stockings and bandages is essential.
184
What additional management strategies are recommended for venous ulcers?
Leg elevation, mobility encouragement, moist wound dressings, and nutrition support are recommended.
185
What should be monitored in patients with venous ulcers?
Infection should be monitored and treated if needed.
186
What does 'itis' mean?
'itis' means 'inflammation'
187
What does 'carditis' mean?
'carditis' means 'inflammation of the heart'
188
What is pericarditis?
Pericarditis is inflammation of the pericardium
| Mainly treated with NSAIDs heals on own
189
What is myocarditis?
Myocarditis is inflammation of the heart muscle
| Mainly treated with NSAIDs , heals on own
190
What is endocarditis?
Endocarditis is inflammation of the endocardium
191
What is infective endocarditis?
Infection of heart valves or endocardial surface.
## Footnote
Previously called 'bacterial endocarditis' – now includes fungi & viruses.
192
What heart valves are often affected by infective endocarditis?
Often affects heart valves, especially mitral and aortic.
193
How has mortality from infective endocarditis changed?
Mortality has improved with antibiotics, but it is still serious.
194
How is infective endocarditis classified?
Classified by left/right-sided, prosthetic/native valve, and device-related.
195
What are the two types of associations in infective endocarditis?
Community vs. health care–associated.
196
What are the main pathogens associated with Infective Endocarditis?
Staph aureus, Strep viridans, Enterococci
197
How can pathogens enter the bloodstream in Infective Endocarditis?
Via dental work, IV drug use, surgery, infected devices
198
What are the major risk factors for Infective Endocarditis?
Prosthetic valves, prior IE, congenital heart defects, IV drug use
199
What is a major complication of Infective Endocarditis?
Valve destruction leading to heart failure
200
What can vegetations in Infective Endocarditis lead to?
Systemic emboli affecting the brain, lungs, and kidneys
201
What are the symptoms of Infective Endocarditis?
Fever, fatigue, weight loss, murmurs, petechiae
202
What are the classic signs of Infective Endocarditis?
Osler’s nodes, Janeway lesions, Roth’s spots
203
What diagnostics are used for Infective Endocarditis?
Blood cultures (x2), echocardiogram, CBC, ESR/CRP
204
What are the nursing priorities for Infective Endocarditis?
Monitor for emboli, HF, infection signs
## Footnote
IV antibiotics (4–6 weeks), Patient education: oral hygiene, follow-up, prophylaxis
205
What is this?
Osler Node
206
What is this?
Janeway lesions
207
What is this?
Roth Spots
208
What is this?
Splinter hemorrhage
209
210
What is Acute Pericarditis?
Inflammation of the pericardial sac.
211
What are the signs and symptoms of Acute Pericarditis?
Chest pain 'pleuritic', pericardial friction rub, change in breathing pattern.
212
How is Acute Pericarditis diagnosed?
EKG changes, CXR, CT.
213
What is the focus of care for Acute Pericarditis?
Manage patient pain & anxiety, rest, medications.
214
What are the complications of Acute Pericarditis?
Pericardial effusion, cardiac tamponade are life-threatening.
215
What is a sign of cardiac tamponade in Acute Pericarditis?
Narrow pulse pressure.
216
What is the treatment for cardiac tamponade?
Pericardiocentesis.
217
What is acute pericarditis?
Acute pericarditis is a condition caused by inflammation of the pericardial sac (the pericardium).
218
What are the components of the pericardium?
The pericardium is composed of the inner serous membrane (visceral pericardium) and the outer fibrous layer (parietal pericardium).
219
What is the pericardial space?
The pericardial space is the cavity between the visceral and parietal layers, containing 10 to 30 mL of serous fluid in a normal state.
220
What functions does the pericardium serve?
The pericardium anchors the heart, provides lubrication to decrease friction, and prevents excessive dilation during diastole.
221
What are the common causes of acute pericarditis?
Common causes include idiopathic origins, viral infections (especially coxsackievirus B), bacterial infections, fungal infections, acute myocardial infarction, tuberculosis, neoplasms, autoimmune conditions, medication reactions, metabolic disorders, and trauma.
222
What distinguishes acute pericarditis from Dressler's syndrome?
Acute pericarditis occurs within 48 to 72 hours after an MI, while Dressler's syndrome appears 4 to 6 weeks after an MI.
223
What is the characteristic pathological finding in acute pericarditis?
An inflammatory response with an influx of neutrophils, increased pericardial vascularity, and fibrin deposition on the visceral pericardium.
224
What are the clinical manifestations of acute pericarditis?
Characteristic manifestations include severe, sharp, pleuritic chest pain that worsens with deep inspiration and lying supine, and is relieved by sitting upright.
225
How can chest pain from pericarditis be differentiated from angina?
Pain from pericarditis can radiate to the trapezius muscle due to phrenic nerve innervation, making it distinct from angina.
226
What is the hallmark finding in acute pericarditis?
The hallmark finding is the pericardial friction rub, a scratching, grating sound from friction between the pericardial and epicardial surfaces.
227
Where is the pericardial friction rub best heard?
It is best heard at the lower left sternal border with the patient leaning forward.
228
How can one differentiate between a pericardial and pleural friction rub?
If the rub is still heard when the patient holds their breath, it is likely cardiac.
229
What percentage of people with chest pain in the emergency department are diagnosed with pericarditis?
Pericarditis is diagnosed in 5% of people presenting to the emergency department with chest pain.
230
What are the diagnostic methods for Acute Pericarditis?
• History and physical examination
• Auscultation of chest
• ECG
• Laboratory: CRP, ESR, white blood cell count, BUN, serum creatinine
• TB test
• Chest radiographic examination
• Echocardiogram
• Pericardiocentesis
• Pericardial biopsy
• CT scan
• Cardiac nuclear scan
231
What are the interprofessional therapies for Acute Pericarditis?
• Treatment of underlying disease
• Bed rest
• ASA (Aspirin)
• NSAIDs
• Colchicine
• Corticosteroids
• Pericardiocentesis (for large pericardial effusion or tamponade)
• Pericardial window (for tamponade or ongoing pericardial effusion)
232
What percentage of infective endocarditis (IE) cases is now accounted for by Rheumatic Carditis/Rheumatic Heart Disease?
Rheumatic Carditis/Rheumatic Heart Disease now accounts for only 20% of IE cases.
233
What condition has Rheumatic Fever caused in heart valves?
Rheumatic Fever has permanently damaged the heart valves.
234
What are the consequences of damaged heart valves due to Rheumatic Fever?
The valves are inflamed, scarred, so they may become narrow or leak.
235
When may heart valve damage begin after a streptococcal infection?
Heart valve damage may start shortly after untreated or undertreated streptococcal infection, such as strep throat or scarlet fever.
236
What causes the inflammatory condition leading to valve damage in Rheumatic Heart Disease?
An immune response causes an inflammatory condition in the body, resulting in ongoing valve damage.
237
What are the disorders associated with the Mitral Valve?
Stenosis, Regurge, Prolapse
238
What are the disorders associated with the Aortic Valve?
Stenosis, Regurge
239
What are the diagnostic methods for heart valve problems?
History and physical examination, CXR, 12 lead ECG, Echocardiogram, Cardiac catheterization, CBC
240
What is the treatment for heart valve problems?
Low Na diet, cardiac medications, diuretics, β-Adrenergic blockers, antidysrhythmic medications, anticoagulation therapy
241
What are examples of cardiac medications used in treatment?
Diuretics, β-Adrenergic blockers, antidysrhythmic medications
## Footnote
Refer to Table 35.8 for details.
242
What is the approach to treating heart valve problems?
Either fix the valve or replace it with a new valve
243
What are the two types of surgical approaches for heart valve treatment?
Minimally invasive (percutaneous) or very invasive (open heart surgery)
244
What is percutaneous transluminal balloon valvuloplasty?
A minimally invasive procedure to treat heart valve problems
245
What is percutaneous valve replacement?
A procedure to replace a heart valve using a minimally invasive approach
246
Where is the mitral valve located?
On the left side of the heart, between the left atrium (LA) and left ventricle (LV).
247
What does the mitral valve control?
It controls the flow of oxygen-rich blood from the lungs into the heart.
248
How many leaflets/flaps does the mitral valve have?
The mitral valve has 2 leaflets/flaps.
249
What is the risk involved in mitral valve surgery?
The risks are quite low.
250
What is mitral valve stenosis?
A condition where the mitral valve narrows, affecting blood flow.
251
What procedure is often done for mitral valve stenosis?
Balloon valvuloplasty is often performed.
252
What is mitral valve regurge?
A condition where the valve 'prolapses', causing backward flow of blood.
253
What is the most common heart valve abnormality?
Mitral valve regurge is the most common heart valve abnormality.
254
What rhythm disturbances may occur with mitral valve problems?
May have rhythm disturbances such as tachycardia or atrial fibrillation (A Fib).
255
What is the most common cause of adult mitral valve stenosis?
Most cases result from rheumatic heart disease, particularly prevalent in low-income countries.
256
What is a common cause of degenerative calcific mitral stenosis?
It is more common in older patients.
257
What are less common causes of mitral valve stenosis?
Congenital mitral stenosis, rheumatoid arthritis, and systemic lupus erythematosus.
258
What structural changes occur due to rheumatic endocarditis?
Scarring of the valve leaflets and chordae tendineae, leading to contractures and adhesions between the commissures.
259
What is the consequence of structural deformities in mitral stenosis?
They cause obstruction of blood flow and create a pressure difference between the left atrium and left ventricle during diastole.
260
What happens to left atrial pressure and volume in chronic mitral stenosis?
They elevate, causing increased pulmonary vasculature pressure and hypertrophy of the pulmonary vessels.
261
What is the primary symptom of mitral stenosis?
Exertional dyspnea due to reduced lung compliance.
262
What other symptoms may occur with mitral stenosis?
Fatigue and palpitations from atrial fibrillation.
263
What heart sounds are associated with mitral stenosis?
A loud first heart sound and a low-pitched, rumbling diastolic murmur, best heard at the apex.
264
What rare symptoms may occur in mitral stenosis patients?
Hoarseness, hemoptysis, chest pain, seizures, or stroke from emboli.
265
What can cause emboli in mitral stenosis?
Blood stasis in the left atrium.
266
Condition: Mitral valve stenosis
Clinical Manifestations: Exertional dyspnea, hemoptysis; fatigue; palpitations; loud, accentuated S1; opening snap; low-pitched, rumbling diastolic murmur.
## Footnote
Electrocardiogram: Right axis deviation, left atrial enlargement, right ventricular hypertrophy, P mitrale (wide, M-shaped P wave), atrial flutter or fibrillation. Echocardiogram: Restricted movement of mitral valve leaflets; decreased size of orifice; diastolic turbulence. Cardiac Catheterization: Left atrial pressure increased at end of diastole, reduction in CO.
267
Condition: Mitral valve regurgitation (Acute)
Clinical Manifestations: Generally poorly tolerated with fulminating pulmonary edema and shock developing rapidly; systolic murmur.
## Footnote
Electrocardiogram: Left atrial enlargement, atrial fibrillation. Echocardiogram: Hyperdynamic left ventricular contraction in association with shock; regurgitant jets and flail chordae or leaflets. Cardiac Catheterization: Contrast medium injection in left ventricle showing regurgitation of blood into left atrium.
268
Condition: Mitral valve regurgitation (Chronic)
Clinical Manifestations: Weakness, fatigue, exertional dyspnea, palpitations; an S3 gallop, holosystolic or pansystolic murmur.
## Footnote
Electrocardiogram: P mitrale, left ventricular hypertrophy, atrial flutter or fibrillation. Echocardiogram: Left atrial enlargement; left ventricular hypertrophy; flail leaflets. Cardiac Catheterization: Contrast medium injection in left ventricle showing regurgitation of blood into left atrium.
269
Condition: Mitral valve prolapse
Clinical Manifestations: Palpitations, dyspnea, chest pain, activity intolerance, syncope; mobile midsystolic nonejection click and a late or holosystolic murmur.
## Footnote
Electrocardiogram: Usually normal; occasionally T-wave inversion or biphasicity in leads II, III, and aVF are noted; PVCs and tachydysrhythmias possible. Echocardiogram: On the M-mode echocardiogram, late-systolic posterior motion or holosystolic billowing of the mitral leaflets; on two-dimensional echocardiogram, systolic billowing of the mitral leaflets. Cardiac Catheterization: Left ventricular angiogram reveals mitral leaflets with prominent scalloping as the leaflets billow into the left atrium during systole.
270
Condition: Aortic valve stenosis
Clinical Manifestations: Angina pectoris, syncope, heart failure, normal or soft S1, prominent S4, crescendo–decrescendo murmur.
## Footnote
Electrocardiogram: Left ventricular hypertrophy, left bundle branch block, complete atrioventricular heart block. Echocardiogram: Restricted movement of aortic valve; diminished orifice; systolic turbulence. Cardiac Catheterization: Left ventricular systolic pressure increased, reduction in CO.
271
Condition: Aortic valve regurgitation (Acute)
Clinical Manifestations: Abrupt onset of profound dyspnea, transient chest pain, progression to shock.
## Footnote
Electrocardiogram: Left ventricular strain. Echocardiogram: Normal-sized left ventricle with hyperdynamic systolic contraction; aortic dissection can be seen, if cause of acute process. Cardiac Catheterization: Significant elevation of left ventricular diastolic pressure.
272
Condition: Aortic valve regurgitation (Chronic)
Clinical Manifestations: Fatigue, exertional dyspnea; water-hammer pulse; heaving precordial impulse; diastolic high-pitched soft decrescendo diastolic murmur, characteristic Austin Flint.
## Footnote
Electrocardiogram: Left ventricular hypertrophy. Echocardiogram: Enlarged left ventricle and dilated aortic root. Cardiac Catheterization: Increase in left ventricular diastolic pressure, aortic root contrast medium injection demonstrating.
273
Condition: Tricuspid stenosis and regurgitation
Clinical Manifestations: Peripheral edema, ascites, hepatomegaly; diastolic low-pitched decrescendo murmur with increased intensity during inspiration (stenosis); pansystolic murmur with increased intensity at inspiration (regurgitation).
## Footnote
Electrocardiogram: Tall, peaked P waves; atrial fibrillation. Echocardiogram: Right ventricular dilation and paradoxical septal motion; usually poor visualization of tricuspid valve itself. Cardiac Catheterization: Pressure gradient across tricuspid valve and increased right atrial pressure (stenosis); reflux of contrast medium into right atrium (regurgitation).
274
What is the function of the aortic valve?
Controls blood flow from the lower left chamber to the aorta, preventing blood from flowing back to the left ventricle. It has 3 leaflets/flaps.
275
What is aortic valve stenosis?
A condition where the aortic valve narrows, affecting blood flow.
276
What should be noted about nitroglycerin in relation to aortic valve problems?
Avoid or use with caution as it can cause severe low blood pressure.
277
What is aortic valve regurgitation?
A condition where the aortic valve does not close properly, allowing blood to flow backward into the heart.
278
What is Mitral Valve Prolapse?
Abnormality of the mitral valve leaflets and the papillary muscles or chordae that allows the leaflets to prolapse, or buckle, back into the left atrium during systole.
279
What medications are used for Mitral Valve Prolapse?
Take medications as prescribed (e.g., β-adrenergic blockers to control palpitations, chest pain)
## Footnote
Example: β-adrenergic blockers help manage symptoms.
280
What nutritional advice is given for Mitral Valve Prolapse?
Adopt healthy eating patterns, avoid caffeine because it is a stimulant and may exacerbate symptoms.
281
When should you seek medical attention for Mitral Valve Prolapse?
If symptoms develop or worsen (e.g., palpitations, fatigue, shortness of breath, anxiety)
## Footnote
Example: Worsening palpitations may require immediate attention.
282
What is Aortic Stenosis?
Congenital OR calcification of aortic valve (similar to CAD).
283
What medications are used for Aortic Stenosis?
Symptom control meds: Diuretics, Antihypertensives.
284
What nutritional advice is given for Aortic Stenosis?
Nothing specific.
285
When should you seek medical attention for Aortic Stenosis?
If symptoms worsen. Surgical valve replacement if severe stenosis PLUS SYMPTOMS!!
286
What does 'fix' or repair the valve refer to?
Valvuloplasty, Percutaneous Transluminal Balloon Valvuloplasty, Open surgical valvuloplasty, Commissurotomy (valvulotomy), Direct vision (open) approach, Closed approach, Annuloplasty 'annulus'
287
What are the two options for valve replacement?
Biologic and mechanical
288
What should be considered when choosing between biologic and mechanical valves?
There are pros/cons to each; what is best for the patient?
289
What are the pros of Biological Valves (Tissue Valves)?
Don’t usually require lifelong anticoagulation (blood thinners).
Lower risk of blood clots compared to mechanical valves.
More “natural” flow dynamics and less chance of valve noise.
290
What are the cons of Biological Valves (Tissue Valves)?
Shorter lifespan: typically last 10–20 years (sometimes less in younger patients).
Higher chance of structural deterioration over time, especially in younger, more active patients.
May eventually require another valve replacement.
291
Who are Biological Valves (Tissue Valves) best for?
Older patients (usually >65–70 years), since the valve will likely last the rest of their lifetime.
Patients who cannot tolerate anticoagulation (e.g., high fall risk, bleeding disorders, contraindications to warfarin).
Women of childbearing age who want to avoid warfarin during pregnancy.
292
What are the pros of Mechanical Valves?
Very durable: can last 20–30+ years (often lifelong).
Ideal for younger patients who would otherwise outlive a tissue valve.
293
What are the cons of Mechanical Valves?
Require lifelong anticoagulation (usually warfarin) to prevent clots.
Increased bleeding risk due to anticoagulation.
Can be associated with audible clicking sounds from the valve.
Higher risk of thromboembolism if anticoagulation isn’t maintained properly.
294
Who are Mechanical Valves best for?
Younger patients (<60 years), since they need durability.
Patients who already require anticoagulation for other reasons (e.g., atrial fibrillation, mechanical prostheses elsewhere).
Those who can reliably maintain INR monitoring and tolerate anticoagulation.
295
What is the goal of treating Dilated Cardiomyopathy?
Controlling heart failure by enhancing myocardial contractility and decreasing afterload.
296
What therapies are used to alleviate symptoms of Dilated Cardiomyopathy?
Drug and nutritional therapy, cardiac rehabilitation, and nonpharmacological therapies.
297
What types of nursing care are involved in the management of Dilated Cardiomyopathy?
Home health and hospice nursing.
NURS 3512
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