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Pathophysiology & Pharmacology 218 > Alterations in Cardiovascular Status (Week 2) > Flashcards

Alterations in Cardiovascular Status (Week 2) Flashcards

1
Q

The symptoms of coronary artery disease manifest as:

A

1) Stable Angina

2) Unstable Angina 3) Myocardial Infarction

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2
Q

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

A

acute coronary syndrome.

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3
Q

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

A

atherosclerosis

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4
Q

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

A

Atheroma

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5
Q

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

A

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.

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6
Q

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

A

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

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7
Q

What happens in atherosclerosis?

A

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.

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8
Q

What happens after the endothelium becomes damaged in Atherosclerosis?

A

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.

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9
Q

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

A

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

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10
Q

The first, “fatty streak” stage of CAD

A

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.

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11
Q

The second, “raised fibrous plaque” stage of CAD

A

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.

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12
Q

The third, “complicated lesion” stage of CAD

A

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.

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13
Q

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

A

collateral circulation

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14
Q

Describe collateral circulation?

A

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.

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15
Q

Primary (modifiable) risk factors for CAD:

A

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

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16
Q

What are some unmodifiable risk factors of CAD?

A

age, sex, and genetic predisposition

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17
Q

Modifiable risk factors are further sub classified as?

A

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.

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18
Q

The five most significant major modifiable risk factors are:

A

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

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19
Q

Seven types of serum lipids:

A

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.

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20
Q

How is CAD onset promoted with elevated serum levels?

A

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.

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21
Q

How is CAD onset promoted with hypertension?

A

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.

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22
Q

How is CAD onset promoted with tobacco use?

A

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.

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23
Q

How is CAD onset promoted with physical inactivity?

A

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

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24
Q

How is CAD onset promoted with obesity?

A

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.

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25
Q

How is CAD onset promoted with diabetes mellitus?

A

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

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26
Q

How is CAD onset promoted with homocysteine?

A

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.

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27
Q

What is metabolic syndrome a combination of?

A

1) Abdominal obesity.
2) Hypertension.
3) Elevated serum-lipid levels.
- and-
4) Elevated blood glucose.

this appears to promote the development of CAD

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28
Q

How is CAD onset promoted with psychological states?

A

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.

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29
Q

What are 3 ways to prevent CAD?

A

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

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30
Q

What is exercise therapy?

A

Exercise helps to increase serum-HDLs and lowers obesity.

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31
Q

What is nutritional therapy?

A

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.

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32
Q

What is drug therapy?

A

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.

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33
Q

Cholesterol medications take three forms:

A

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.

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34
Q

What is angina and what is it caused by?

A

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

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35
Q

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

A

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

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36
Q

Why does ischemia occur?

A

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).

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37
Q

What is the pain of angina caused by?

A

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.

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38
Q

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

A

20 minutes.

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39
Q

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

A

“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.

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40
Q

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

A

silent ischemia

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41
Q

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

A

Nocturnal angina

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42
Q

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

A

Angina decubitus

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43
Q

_________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.

A

Prinzmetal’s angina (aka “variant angina”)

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44
Q

Treatment of Chronic Stable Angina.

A

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

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45
Q

Nitrates

A

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.

46
Q

Beta-blockers

A

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

47
Q

Calcium-channel blockers

A

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.

48
Q

Angiotensin converting enzyme (ACE) inhibitors

A

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

49
Q

Acute Coronary Syndrome?

A

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.

50
Q

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

A 
unstable angina (UA). 
Unlike stable angina, unstable angina is unpredictable and represents a medical emergency.
51
Q

___________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.

A

A myocardial infarction

52
Q

Myocardial infarctions are classified according to?

A

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.

53
Q

The innermost layer of heart tissue is called?

A

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.

54
Q

The clinical manifestations of an MI include:

A

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

55
Q

Describe the pain that comes with MI’s.

A

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.

56
Q

Describe SNS stimulation that comes with MI’s.

A

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.

57
Q

Describe cardiovascular manifestations that come with MI’s.

A

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.

58
Q

Describe the cardiovascular manifestations that come with MI’s.

A

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.

59
Q

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

A

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

60
Q

Describe the fever that comes with MI’s.

A

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

61
Q

What happens in the event of an MI?

A

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.

62
Q

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

A

changes in ECG values, affected areas.

63
Q

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

A

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

64
Q

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

A

the damage was only partialthickness.

65
Q

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

A

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.

66
Q

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

A

late heart failure.

67
Q

Complications of MI’s.

A 
Dysrhythmias
Ventricular fibrillation
Heart failure
Cardiogenic shock
Papillary muscle dysfunction
Ventricular aneurism
Pericarditis
Dressler’s syndrome
68
Q

Dysrhythmias

A

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.

69
Q

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

A

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

70
Q

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

A

papillary muscle dysfunction.

71
Q

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?

A

ventricular aneurism.

72
Q

Dressler’s syndrome

A

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.

73
Q

Diagnostics for MI

A

ECG’s and serum-marker blood tests.

74
Q

What are serum-marker blood tests used to determine?

A

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).

75
Q

Coronary angiography

A

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.

76
Q

Collaborative care for MI’s.

A

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

77
Q

Percutaneous coronary intervention

A

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.

78
Q

Coronary artery bypass grafts (CABGs)

A

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.

79
Q

Fibrinolytic therapy

A

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.

80
Q

Drug Therapy for ACS

A

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.

81
Q

Nursing considerations for MI.

A

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.

82
Q

Sudden Cardiac Death

A

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).

83
Q

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

A

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).

84
Q

Intermittent claudication

A

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).

85
Q

Signs of PAD include:

A

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

86
Q

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

A

elevating PAD-affected limbs

87
Q

As PAD develops, what happens?

A

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.

88
Q

A possible serious complication of PAD?

A

Gangrene.

89
Q

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

A

ankle-brachial index (ABI)

90
Q

What is ankle-brachial index (ABI)?

A

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.

91
Q

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

A

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

92
Q

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

A

PAD

93
Q

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

A

PAD

94
Q

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

A

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

95
Q

Balloon angioplasty is occasionally used in select clients with___________.

A

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

96
Q

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

A

Peripheral arterial bypass grafts

97
Q

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

A

Amputation.

98
Q

What are some examples of Venous Disorders.

A

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

99
Q

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

A

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.

100
Q

Three major factors that affect the development of VTE are:

A

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).

101
Q

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

A

“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.

102
Q

Thrombophlebitis

A

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

103
Q

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 ___________.

A

Venous return

Edema

104
Q

____________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.

A

Exercise.

105
Q

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

A

Compression devices

Stockings

106
Q

Surgical intervention for DVTs involves?

A

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

107
Q

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.

A

arterial problems.

108
Q

Varicose Veins

A

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.

109
Q

Surgical intervention for varicose veins involves?

A

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

110
Q

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?

A

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

Pathophysiology & Pharmacology 218 (20 decks)

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