Alterations in Cardiovascular Status (Week 2)

Question 1

The symptoms of coronary artery disease manifest as:

Answer 1

1) Stable Angina

2) Unstable Angina 3) Myocardial Infarction

Question 2

Unstable angina (UA) and myocardial infarction are the more serious of the three forms of CAD, and are also called?

Answer 2

acute coronary syndrome.

Question 3

Coronary artery occurs through the development of ____________ in the coronary vessels and involves reduced or obstructed flow of blood to myocardial tissues.

Answer 3

atherosclerosis

Question 4

_________refers to the area of a blood vessel that has atherosclerotic damage.

Answer 4

Atheroma

Question 5

Terms used to describe the disease process of atherosclerosis in the coronary arteries are:

Answer 5

1) Arteriosclerotic heart disease (ASHD)
2) Cardiovascular heart disease (CVHD)
3) Ischemic heart disease (IHD)
4) Coronary heart disease (CHD)
5) And of course… Coronary artery disease.

Question 6

Atherosclerosis begins with damage to CV endothelial tissues. Damage to our vessel walls can come from a number of sources:

Answer 6

1) Hypertension
2) Tobacco Use
3) Hyperlipidemia
4) Hyperhomocysteinemia (elevation of a homocysteine, an amino acid)
5) Hemodynamic Factors (factors relating to the movement of blood in the body) 6) Diabetes
7) Infections
8) Immune Reactions

Question 7

What happens in atherosclerosis?

Answer 7

The plaques that obstruct circulation are deposits composed of cholesterol and lipid materials. They are formed as components of the blood interact with the vascular wall and become calcified over time.

Question 8

What happens after the endothelium becomes damaged in Atherosclerosis?

Answer 8

It will interact with platelets. Somehow, the damaged vessel wall causes the platelets to “activate” and release a growth factor that stimulates smooth muscle proliferation. The smooth muscle grows on the endothelium and entraps lipid materials. As these lipids become calcified, they act as an irritant to the vascular linings. Platelets adhere to the calcified fatty deposits and aggregate. Clotting factors are released from the blood at these deposits and thrombi can occur.

Question 9

Coronary artery disease takes years to develop, and occurs in three phases:

Answer 9

1-Fatty Streak, 2-Raised Fibrous Plaque, 3-Complicated Lesion

Question 10

The first, “fatty streak” stage of CAD

Answer 10

is identifiable as a layer of fatty smooth muscle grown in the damaged endothelial tissue. The high lipid-content of this tissue gives it a yellowish tinge.

Question 11

The second, “raised fibrous plaque” stage of CAD

Answer 11

As the fatty streak grows, it begins to damage the surrounding epithelium. When this happens, cholesterol and lipids are shuttled into the most superficial vascular layer, the tunica intima, and fatty deposits form. Additionally, the clotting factors released from platelet aggregations cause the formation of a fibrous, collagenic outer layer, giving it a greyish or whitish appearance. This fibrous plaque causes inflammation to its surrounding tissues.

Question 12

The third, “complicated lesion” stage of CAD

Answer 12

Over time, the inflammation in the tissues surrounding the fibrous plaque deposit cause the plaque deposit to become unstable, and it can ulcerate and rupture. Essentially, this looks like the inner wall of the coronary vessel bursting out into the vessel lumen. Platelets adhere to these ruptured tissues and a thrombus is formed. The thrombus can adhere to the vascular wall and further restrict or totally occlude blood flow.

Question 13

The human body can adapt to coronary artery disease through the development of?

Answer 13

collateral circulation

Question 14

Describe collateral circulation?

Answer 14

As a vessel becomes occluded, a network of several smaller blood vessels will grow from one side of the plaque deposit to the other, creating a “plaque-deposit-bypass” that reroutes blood flow. As such, the debilitating symptoms of CAD will be reduced or avoided depending on the rate of progression of the plaque deposit; these new vascular networks take time to form. The severity of symptoms with CAD depends in the rate of its onset.

Question 15

Primary (modifiable) risk factors for CAD:

Answer 15

1) Smoking
2) Hypertension
3) Diabetes
4) Abdominal Obesity
5) Inadequate fruit and vegetable intake.
6) Alcohol Consumption
7) Inactivity

Question 16

What are some unmodifiable risk factors of CAD?

Answer 16

age, sex, and genetic predisposition

Question 17

Modifiable risk factors are further sub classified as?

Answer 17

Major or contributing, depending on whether research has precisely determined the significance and prevalence of the particular risk factor in CAD onset If these determinations have been made, they are known as major modifiable risk factors. If they haven’t they are called contributing modifiable risk factors.

Question 18

The five most significant major modifiable risk factors are:

Answer 18

1) Elevated serum lipid levels.
2) Hypertension
3) Tobacco Use
4) Physical Inactivity
5) Obesity

Question 19

Seven types of serum lipids:

Answer 19

1&2) Low-, very low-, and high-density lipoproteins (LDLs/VLDLs/HDLs) are types of cholesterol. 3,4,5) Saturated, monounsaturated and polyunsaturated fats are serum-triglycerides.
6) Phospholipids.

Question 20

How is CAD onset promoted with elevated serum levels?

Answer 20

It is promoted when LDLs and serum-triglycerides are both chronically high. In the blood, these particles combine and form the very low-density lipoproteins, which are the major contributor to plaque formations.

Question 21

How is CAD onset promoted with hypertension?

Answer 21

Chronically high blood pressures (>140 systolic) exhibit shearing forces on vascular endothelium. This damaged endothelium will see the buildup of atherosclerotic plaques which begin to reduce blood flow volumes. As the heart compensates for this reduced blood flow by increasing contraction force or rate, blood pressure is increased even further.

Question 22

How is CAD onset promoted with tobacco use?

Answer 22

Smoking raises blood pressure and nicotine can cause platelet adhesion in the blood leading to the formation of an embolus (circulating blood clot) these circulating clots. Also, the inhaled carbon monoxide from smoking tobacco is believed to be a chemical irritant that damages the endothelium.

Question 23

How is CAD onset promoted with physical inactivity?

Answer 23

Exercise promotes higher HDL levels and better development of collateral circulation, and it reduces obesity.

Question 24

How is CAD onset promoted with obesity?

Answer 24

With obesity, the increased vasculature of the adipose tissues makes the heart work much harder, and over time it becomes enlarged, increasing its oxygen demands and raising blood pressure. Additionally, obesity can lead to diabetes mellitus and vascular complications.

Question 25

How is CAD onset promoted with diabetes mellitus?

Answer 25

Diabetic individuals typically have elevated serum-lipid levels (hyperlipidemia). Also, vascular damage promotes the formation of fatty streaks.

Question 26

How is CAD onset promoted with homocysteine?

Answer 26

This particular amino acid is a product of dietary protein metabolism and damages endothelial linings, promoting the buildup of fatty plaques. Its levels can be reduced with the supplementation of B-complex (6, 12, folic acid) vitamins.

Question 27

What is metabolic syndrome a combination of?

Answer 27

1) Abdominal obesity. 2) Hypertension. 3) Elevated serum-lipid levels. - and- 4) Elevated blood glucose. *this appears to promote the development of CAD*

Question 28

How is CAD onset promoted with psychological states?

Answer 28

The perfectionist, stress-driven people with type A personalities are shown to be at increased risk of developing CAD. Stress, in general, promotes the development of CAD with “the stress response.” Elevated blood pressures and increased serum-glyceride and lipid levels foster atherogenesis. Also, the increased circulating catecholamines (epinephrine / norepinephrine) are believed to cause endothelial damage. People with depression also have elevated catecholamines and, as such, are also predisposed to developing CAD.

Question 29

What are 3 ways to prevent CAD?

Answer 29

1) Exercise therapy 2) Nutritional therapy 3) Drug therapy

Question 30

What is exercise therapy?

Answer 30

Exercise helps to increase serum-HDLs and lowers obesity.

Question 31

What is nutritional therapy?

Answer 31

Peoples’ diets should be looked at to lower LDL cholesterol and serum-triglycerides. Omega-3 fatty acids have been shown to reduce the risks of CAD when consumed regularly.

Question 32

What is drug therapy?

Answer 32

Individuals with a serum-cholesterol level of 5.2mmol/L or higher should be treated. If diet and exercise cannot correct their cholesterol level, they should be administered a cholesterol-therapy medication.

Question 33

Cholesterol medications take three forms:

Answer 33

1) Drugs that restrict lipoprotein production. Statins reduce serum-cholesterol by preventing the liver from synthesizing it. Additionally, it increases the ability of the liver to filter LDLs out of the blood. 2) Drugs that increase lipoprotein removal. The liver converts blood-cholesterol to bile acids. Some drugs increase the body’s production of bile acid, lowering serum-cholesterol. 3) Drugs that decrease cholesterol absorption. Some medications reduce the amount of dietary lipidabsorption.

Question 34

What is angina and what is it caused by?

Answer 34

Angina is chest pain and it is caused by myocardial ischemia.

Question 35

What is Chronic Stable Angina and what is it a manifestation of?

Answer 35

It is chest pain that occurs intermittently over time, with the same onset, duration, and intensity and it is a manifestation of CAD.

Question 36

Why does ischemia occur?

Answer 36

Ischemia occurs when there is an inadequate blood supply to a specific part of the body. Thus, as coronary atherosclerosis narrows the arteries of the heart, myocardial ischemia occurs, especially when there is an increased workload on the heart. Ischemia causes hypoxia in the affected tissue(s).

Question 37

What is the pain of angina caused by?

Answer 37

The pain of angina is caused by lactic acid irritating myocardial nerves when hypoxic tissues begin anaerobic respiration in their attempt to survive. Because the nerves are connected through the upper thoracic region, particularly in the right shoulder, referred pain often occurs. The referred pain of angina can also be felt on the jaw, down the arms, or between their shoulder blades on their back.

Question 38

Once a vessel becomes ischemic, how long do the tissues they are supplying have before they start to die?

Answer 38

20 minutes.

Question 39

People experiencing angina may describe their chest “pain” as?

Answer 39

“Pressure” or “an ache.” It is rarely sharp or stabbing. The pain of angina usually lasts for 3-5 minutes. As such, it serves as a protective mechanism; the angina is caused by exertion and the pain prevents the individual from continuing exertion. Under the lower oxygen-demand level, the tissues are once again adequately oxygenated, lactic acid disperses, and the pain subsides.

Question 40

In the event of nerve damage such as with diabetic neuropathy, the angina from the ischemia will not be felt. This is called?

Answer 40

silent ischemia

Question 41

__________ occurs at night but not necessarily when the individual is lying down or sleeping.

Answer 41

Nocturnal angina

Question 42

__________occurs when the person is lying down. It is usually relieved by standing or sitting.

Answer 42

Angina decubitus

Question 43

_________is a rare form of angina that occurs from intermittent vascular spasm of coronary arteries. Although it can occur in people with CAD, it is not necessarily associated with the disease.

Answer 43

Prinzmetal’s angina (aka “variant angina”)

Question 44

Treatment of Chronic Stable Angina.

Answer 44

The treatment of CSA involves decreasing the tissue oxygen demand and/or increasing available oxygen. It is usually mediated through pharmacotherapy. 1) Nitrates 2) Beta-blockers 3) Calcium-channel blockers 4) Angiotensin converting enzyme (ACE) inhibitors

Question 45

Nitrates

Answer 45

are a common form of angina medication. They act as vasodilators in both the coronary and peripheral vessels. Vasodilation in the heart decreases the potential for ischemia to cause harm. Vasodilating the peripheral vessels serves to increase the volume of blood in the periphery and lowers the volume that the heart is pumping through its shorter circulation routes; the heart doesn’t need to work as hard. Nitrates can be sublingual (short-acting) or transdermal (“patches” = long acting). Orthostatic hypertension is a side effect of using nitrate medications.

Question 46

Beta-blockers

Answer 46

decrease the work (contractility) of the heart, lowering its oxygen demand. They are named with a “–lol” suffix.

Question 47

Calcium-channel blockers

Answer 47

decrease heart contractility as well as acting as vasodilators. CCBs have the effect of increasing serum-digoxin levels for people taking both forms of these heart medications. So, people that are on digoxin should be measured for toxicity if they begin using calcium channel blockers.

Question 48

Angiotensin converting enzyme (ACE) inhibitors

Answer 48

are also help to relax blood vessels and are used to treat angina.

Question 49

Acute Coronary Syndrome?

Answer 49

Acute coronary syndrome involves either unstable angina or myocardial infarction, and it is associated with deterioration of a once-stable plaque deposit. The plaque ruptures, a thrombus forms, and blood flow is restricted or occluded.

Question 50

If the onset, duration, or intensity of angina are variable, if it is new, or if it occurs while the individual is at rest, it is considered to be

Answer 50

``` unstable angina (UA). Unlike stable angina, unstable angina is unpredictable and represents a medical emergency. ```

Question 51

___________occurs in the case of myocardial ischemia that is unrelieved. Hypoxic tissues begin to die. They are usually caused by thrombus formation. Dead heart cells can no longer contract, and so the damage that an MI causes corresponds to the area of tissues that the ischemia affects.

Answer 51

A myocardial infarction

Question 52

Myocardial infarctions are classified according to?

Answer 52

Their location on the heart. Either anterior, inferior, posterior, or lateral, or septal. Depending on where the ischemia is occurring, MIs can affect more than one location.

Question 53

The innermost layer of heart tissue is called?

Answer 53

The subendocardium. It is the first to become necrotic in the event of severe ischemia (>20mins). It takes about 4-6 hours of severe ischemia for the full thickness of the affected tissue to die.

Question 54

The clinical manifestations of an MI include:

Answer 54

1) Pain 2) Sympathetic Nervous System Stimulation 3) Cardiovascular Manifestations 4) Nausea and Vomiting 5) Fever

Question 55

Describe the pain that comes with MI's.

Answer 55

Severe, immobilizing chest pain not relieved by rest, position change, or nitrates is the hallmark indication that someone’s experiencing an MI. Weakness and shortness of breath may also occur. Often, this pain will occur earlier in the day. People with (diabetic) neuropathy may not feel the pain and, as such, may not know they’re having an MI.

Question 56

Describe SNS stimulation that comes with MI's.

Answer 56

In an MI, the dying (ischemic) tissues release catecholamines (epi/norepi) that cause systemic effects, it is like an induced “stress response.” Peripheral vasoconstriction may make the person’s skin feel cool to touch.

Question 57

Describe cardiovascular manifestations that come with MI's.

Answer 57

In an MI, the dying (ischemic) tissues release catecholamines (epi/norepi) that cause systemic effects, it is like an induced “stress response.” Peripheral vasoconstriction may make the person’s skin feel cool to touch.

Question 58

Describe the cardiovascular manifestations that come with MI's.

Answer 58

In response to the elevated catecholamines (above), the heart (and BP) will often initially elevate. Then, because of the damage to the heart, cardiac output decreases. If the damage is to the left side of the heart, pulmonary congestion is likely to occur. Also, kidney vasoconstriction reduces perfusion and urine production.

Question 59

Describe the nausea and vomiting that come with MI's.

Answer 59

Epigastric pain (heartburn) is common with angina or myocardial infarction. The (general) pain is severe enough, nausea and vomiting can occur.

Question 60

Describe the fever that comes with MI's.

Answer 60

As myocardial cells die, their released contents cause systemic inflammatory symptoms and can induce a fever.

Question 61

What happens in the event of an MI?

Answer 61

The dying cells release enzymes that serve as diagnostic markers, and they initiate inflammatory processes. Neutrophils and macrophages remove the dying tissue within a few days, making the heart wall of the infected area thinner. The catecholamines released by the dying tissues cause the body to break down fats and glycogen, increasing serum-lipid and glucose levels.

Question 62

The change in cardiac performance is identifiable by __________ which can identify the location of _________.

Answer 62

changes in ECG values, affected areas.

Question 63

If there is an elevated ST interval (STEMI), it indicates?

Answer 63

the infarction tissue damage depth spans the full thickness of the myocardium.

Question 64

If it is non-STEMI (NSTEMI), it indicates?

Answer 64

the damage was only partialthickness.

Question 65

What happens after the necrotic tissues are removed after an MI?

Answer 65

scar tissues form as tissues attempt to repair themselves. It takes some time for the damaged, thinned, myocardial wall to develop scar tissue that is strong enough to resist elevated cardiac demands. For this reason, individuals who experience an MI must not exert themselves for several weeks following.

Question 66

The region of scar tissue is not as compliant (less contractile) than normal heart tissue, and reduces cardiac function. In an attempt to restore cardiac performance, ventricular remodeling including hypertrophy and dilation occur. These changes in heart structure can lead to heart failure much later on, which is known as

Answer 66

late heart failure.

Question 67

Complications of MI's.

Answer 67

``` Dysrhythmias Ventricular fibrillation Heart failure Cardiogenic shock Papillary muscle dysfunction Ventricular aneurism Pericarditis Dressler’s syndrome ```

Question 68

Dysrhythmias

Answer 68

are common (affect 80%) after an MI. They include tachy- and bradycardia and an irregular heartbeat, all of which adversely affect the ischemic myocardium. Ventricular fibrillation is a form of dysrhythmia that can be lethal.

Question 69

Because of the reduction of cardiac performance, the heart may not be able to produce enough blood flow to meet the body’s metabolic demands. When this occurs, it is known as

Answer 69

Heart failure. As the body’s metabolic demands are unmet with heart failure, widespread cardiogenic shock can occur.

Question 70

Papillary muscles are muscles that connect to the heart’s AV valves via chordae tendineae that help the valves function. When the MI damages tissues that contain papillary muscles, reduced AV valve function occurs, and regurgitation across the affected valve causes murmurs and reduces cardiac output. This is known as

Answer 70

papillary muscle dysfunction.

Question 71

When the MI is severe enough, it affects a thicker segment of the myocardial wall, and the remaining tissue (after the necrotic tissues have been removed) is thin. The thinned heart wall can balloon-out, which is known as a?

Answer 71

ventricular aneurism.

Question 72

Dressler’s syndrome

Answer 72

occurs when pericarditis leaks fluid (effusion) and is accompanied by a fever. It is thought to be an antigen-antibody reaction to the dead myocardial cells and can sometimes be detected by elevated white blood cell counts.

Question 73

Diagnostics for MI

Answer 73

ECG's and serum-marker blood tests.

Question 74

What are serum-marker blood tests used to determine?

Answer 74

if an MI occurred are certain proteins called serum cardiac markers that are released from the dying myocardial cells. Cardiac kinase (CK) is one marker that is detectable from 3hrs-3days following an MI, and its levels can indicate the degree of damage that occurred. Additionally, cardiac-specific troponin can be detected by blood testing and are detectible for significantly longer than CK (up to 5-14 days).

Question 75

Coronary angiography

Answer 75

where contrast solution is infused into the beginning of the aorta and circulated through the coronary vessels, and the heart is x-rayed, can produce detailed images that accommodate evaluation of the location and extent of the damage and indicate the best therapeutic methods for recovery.

Question 76

Collaborative care for MI's.

Answer 76

1) Nitroglycerine and aspirin should be administered ASAP 2) morphine can be administered for pain. 3) Oxygen supplementation can offset the degree of damage that occurs to ischemic areas. 4) Percutaneous coronary intervention 5) Coronary artery bypass grafts 6) Fibrinolytic therapy

Question 77

Percutaneous coronary intervention

Answer 77

involves the insertion of an inflatable balloon via catheter that, when inflated, presses the coronary plaques up against the vascular walls, spreading them out and improving circulation. PCI is a nonsurgical intervention, can be performed with local anesthesia, and the client can be home within 1 to 3 days afterwards. They can be back to work in 5-7 days.

Question 78

Coronary artery bypass grafts (CABGs)

Answer 78

can reroute blood flow, artificially, in the same way that collateral circulation does. Stents are hollow tubes that are inserted into ischemic vessels to restore luminal diameter and blood flow.

Question 79

Fibrinolytic therapy

Answer 79

the use of clot-busting medications, can be used to break down and eliminate coronary thrombi. Fibrinolytic medications are always administered via IV and it is important to monitor for bleeding in clients that have healing wounds (surgical or other) because the clot-busting effects are systemic.

Question 80

Drug Therapy for ACS

Answer 80

IV nitroglycerine can be administered to improve coronary circulation and reduce angina. Additionally, the vasodilation in peripheral vessels increases the amount of blood in the periphery and reduces workload of the heart. Many of the drugs used to treat ACS are the same as pharmacotherapy for angina: nitroglycerine, beta-blockers, ACE- inhibitors, and calcium channel blockers reduce the damage caused by an MI. Additionally, antidysrhythmics, cholesterol-lowering drugs, and stool softeners (to reduce constipation from morphine administration) may be used.

Question 81

Nursing considerations for MI.

Answer 81

In the first phases following an acute cardiac complication, the focus of nursing interventions should be on pain assessment and relief, physiological monitoring with vital statistics and other assessment methods, promoting rest, and relieving anxiety. Following the acute phase, patients should be educated on how to lower their risk of developing additional cardiac complications.

Question 82

Sudden Cardiac Death

Answer 82

If an acute cardiac complication causes death, it is known as sudden cardiac death. Sometimes these people can be revived, but most (80%) will have neurological impairment. In cardiac death, the sudden lack of cardiac output causes decreased blood supply to the brain. Death will usually occur within one hour of the initial symptoms (angina, palpitations). Ventricular dysrhythmias are a leading cause of sudden cardiac death (SCD).

Question 83

The arteries that peripheral arterial disease (PAD) affects are:

Answer 83

1) Aortoiliac 2) Femoral ** 3) Popliteal ** these two are the most common in nondiabetic patients. 4) Tibeal 5) Peroneal Diabetic clients typically develop PAD in the lower arteries (below the knee).

Question 84

Intermittent claudication

Answer 84

is periodic, temporary, ischemic muscle pain and is the classic symptom of PAD. The pain is a byproduct of lactic acid buildup in the muscle(s) being deprived of oxygen. In the earlier stages of PAD, pain only occurs open exertion of the particular muscle group. Later on, it happens at rest as well. Pentoxifylline is a drug used to treat intermittent claudication and works by altering blood properties (RBC flexibility, fluid viscosity).

Question 85

Signs of PAD include:

Answer 85

1) Taut, shiny skin. 2) Loss of hair in the affected area. 3) Diminished or absent peripheral pulses.

Question 86

Because PAD is arterial, and gravity aids in increasing arterial blood flow, ________ increases the severity of the symptoms.

Answer 86

elevating PAD-affected limbs

Question 87

As PAD develops, what happens?

Answer 87

the affected limb will atrophy and will heal from any trauma it incurs very slowly. Slow wound healing can result in the development of infection and necrotic tissues, which is the development of ulcers.

Question 88

A possible serious complication of PAD?

Answer 88

Gangrene.

Question 89

A diagnostic test that can reveal the existence and severity of PAD is the?

Answer 89

ankle-brachial index (ABI)

Question 90

What is ankle-brachial index (ABI)?

Answer 90

It is a number calculated by comparing the ratio of systolic blood pressures between the brachial and ankle (posterior tibial) arteries. A healthy ratio is anywhere between 0.9 – 1.3, which means that the blood pressure in the ankle is 90-130% that of the brachial. As PAD reduces the peripheral blood flow, a ratio of 0.41-0.89 indicates mild PAD. 0-0.4 is severe PAD.

Question 91

Prevention and lowering the onset of symptoms of PAD includes the same interventions as with CAD, what are they?

Answer 91

1) Lower hypertension. 2) Quit smoking. 3) Lower serum-lipid levels. 4) Tight BG control with diabetic patients.

Question 92

Antiplatelet agents such as arpirin, ticlopidine, and clopidogrel are effective in lowering the risk of developing?

Answer 92

PAD

Question 93

Mild exercise such as walking is the primary nonpharmacological treatment of?

Answer 93

PAD

Question 94

Treatment of the client with later-stage PAD involves symptom management:

Answer 94

protection from trauma, wound treatment, infection control, etc.

Question 95

Balloon angioplasty is occasionally used in select clients with___________.

Answer 95

Small, localized areas of PAD. Stents can be used in combination with balloon angioplasty.

Question 96

____________are a surgical intervention that can be used to treat areas of PAD.

Answer 96

Peripheral arterial bypass grafts

Question 97

___________is the least desirable but most effective treatment of PAD. It is reserved for cases where no treatment alternative is sufficient.

Answer 97

Amputation.

Question 98

What are some examples of Venous Disorders.

Answer 98

1) venous thromboembolism (VTE) 2) Thrombophlebitis 3) Varicose veins

Question 99

Venous thromboembolism (VTE) is becoming more commonly used than deep venous thrombosis (DVT). What is it?

Answer 99

Although they mean pretty much the same thing, VTEs encompass pulmonary embolisms as well, which makes sense because that’s what DVTs will progress to if left untreated. Pulmonary embolisms are a potentially lethal complication of DVTs.

Question 100

Three major factors that affect the development of VTE are:

Answer 100

1) Venous Stasis (We need our skeletal muscle pump. Also occurs due to malfunctioning vein valves). 2) Damage to the endothelium (Provides location for development of thrombus). 3) Hypercoagulability of the blood (Normal fibrinolytic processes do not dissolve the clot).

Question 101

A common site for the development of DVTs is at the?

Answer 101

“Valve cusps” of veins. These small disturbances of passing blood flow create little “back-eddys” that provide environments allowing for the accumulation of blood products.

Question 102

Thrombophlebitis

Answer 102

Is swelling and hardening of veins and is caused by venous insufficiency (DVTs or Varicose Veins).

Question 103

Although symptoms of limbs with arterial insufficiency worsen with elevation, limbs with venous insufficiency and/or thrombophlebitis can be lifted up to increase__________ and lessen ___________.

Answer 103

Venous return | Edema

Question 104

____________is an effective nonpharmacological treatment for venous insufficiency. Bedridden clients can be urged to dorsiflex there feet and rotate their ankles to enhance skeletal muscle pump mechanisms.

Answer 104

Exercise.

Question 105

___________ such as __________, can be used to minimize the risk of developing DVTs and lessen edema.

Answer 105

Compression devices | Stockings

Question 106

Surgical intervention for DVTs involves?

Answer 106

Venous thrombectomy, which is where an incision in the vein is made to physically remove the clot.

Question 107

Although anticoagulants are not recommended for arterial insufficiency, they are commonly used for venous problems. They are not used for __________because clots aren’t the major issue, reduced blood flow is.

Answer 107

arterial problems.

Question 108

Varicose Veins

Answer 108

Are dilated, bulging, tortuous (twisting and turning) vessels that usually occur in the saphenous system (around the knee and into the lower leg), and they drastically increase the risk of developing a DVT. Individuals with moderate-severe varicose veins are not supposed to fly without using compression stockings. Increased cabin pressures decrease venous blood return and increase the risk of DVTs.

Question 109

Surgical intervention for varicose veins involves?

Answer 109

Ligation (closing off) of the affected vessel. Collateral vessels will accommodate the altered blood flow.

Question 110

With the changes in the vein structure, the valves in the affected area fail to operate properly. Venous return decreases and blood can even backflow. When this happens, what happens?

Answer 110

The increased pressures of the vein compound the advancement of its physical changes (stretching).