Unit 5; Alterations In O2/cardio System

Front 1

Name 3 layers of the heart:

Back 1

1. Endocardium: a thin inner lining
2. Myocardium: a layer of muscle
3. Epicardium: a fibrous outer layer

Front 2

A fibroserous sac that surrounds the heart is:

Back 2

Pericardium Sac

Front 3

The inner layer of the pericardium is in contact with the epicardium:

Back 3

Visceral Layer

Front 4

The outer layer that is in contact with the mediastinum:

Back 4

Parietal Layer

Front 5

Is the right or left ventricle thicker? Why?

Back 5

Left is 2 to 3 times thicker than the right due to the necessity to generate the force needed to pump the blood into the systemic circulation

Front 6

From the body; the right atrium receives blood from:

Back 6

The superior vena cava, inferior vena cava, and coronary sinus

Front 7

Blood passes through this valve from the right atrium to right ventricle:

Back 7

Tricuspid Valve

Front 8

The right ventricle pumps blood through the _____ valve into the _____ ______ and to the ______

Back 8

pulmonic valve; pulmonary artery; lungs

Front 9

Blood flows from the _____ to the left atrium by way of the _______ ______.

Back 9

lungs: pulmonary veins

Front 10

Blood passes through this valve from the left atrium to left ventricle:

Back 10

Mitral valve

Front 11

Blood is ejected by the left ventricle through the _____ valve in to the _____ and enters _______ circulation.

Back 11

aortic valve; aorta; systemic circulation

Front 12

Cusps of the mitral and tricuspid valves are attached to thin strands of fibrous tissue called:

Back 12

chordae tendineae
-These prevent back flow into the atria during ventricular contraction.

Front 13

Name the 2 valves that are also known as semilunar valves:

Back 13

Pulmonic and aortic valves
-These prevent blood from regurgitating into the ventricles at the end of each ventricular contraction.

Front 14

Blood flows into the 2 major coronary arteries during:

Back 14

Diastole or relaxation of myocardium

Front 15

Name the 2 branches of the left coronary artery:

Back 15

1. Left anterior descending artery
2. Left circumflex artery

Front 16

Name the different areas of the heart the left coronary artery supplies:

Back 16

-left artrium
-left ventricle
-interventricular septum
-a portion of the right ventricle

Front 17

Name the different areas of the heart the right coronary artery supplies:

Back 17

-right atrium
-right ventricle
-a portion of the posterior wall of the left ventricle

Front 18

Where does most of the blood from the coronary system drain?

Back 18

Into the coronary sinus, which in turn empties into the right artrium near the entrance to the inferior vena cava

Front 19

Electrical impulse is initiated by:

Back 19

The SA node or "pacemaker of the heart"

Front 20

Describe the path an action potential takes in the heart:

Back 20

1. SA node
2. AV node
3. Bundle of His
4. left and right branches
5. Purkinje Fibers

Front 21

Cardiac cycle starts with:

Back 21

Depolarization of the SA node

Front 22

What and when does absolute refractory period occur?

Back 22

-Occurs during systole; during which cardiac muscle does not respond to any stimuli

Front 23

What and when does relative refractory period occur?

Back 23

Occurs during diastole; during which cardiac muscle recovers

Front 24

Describe the meaning of each wave on an ECG:
P wave:

Back 24

P: begins with the firing of the SA node and represents depolarization of the fibers of the atria

Front 25

Describe the meaning of each wave on an ECG:
QRS complex:

Back 25

QRS: represents depolarization from the AV throughout the ventricles

Front 26

Describe the meaning of each wave on an ECG:
T wave:

Back 26

T: represents repolarization of the ventricles

Front 27

Describe the meaning of each wave on an ECG:
U wave (if seen):

Back 27

U: if seen, may represent repolarization of the Purkinje fibers or it may be associated with hypokalemia

Front 28

Contraction of the myocardium and results in ejection of blood from the ventricles is:

Back 28

Systole

Front 29

Relaxation of the myocardium which allows for filling of the ventricles is:

Back 29

Diastole

Front 30

The amount of blood pumped by each ventricle in 1 minute:

Back 30

Cardiac Output

Front 31

Volume of blood in the ventricles at the end of diastole and before the next contraction; affects the CO by affecting the SV:

Back 31

Preload

Front 32

It determines the amount of stretch placed on myocardial fibers; the greater the stretch results in the greater contraction.

Back 32

Preload

Front 33

Can be increased by norepinephrine and epinephrine released by the sympathetic nervous system; raises the SV by increasing ventricular emptying:

Back 33

Contractility

Front 34

The peripheral resistance against which the left ventricle must pump:

Back 34

Afterload

Front 35

This vessel has thick, elastic walls; cushions the impact of the pressure created by ventricular contraction; contains some smooth muscle:

Back 35

Arteries

Front 36

This vessel has relatively little elastic tissue and more smooth muscle; serves as major control of arterial blood pressure and distribution of blood flow:

Back 36

Arterioles

Front 37

This innermost lining of the arteries serves to maintain hemostasis, promote blood flow, and under normal conditions, inhibits blood coagulation:

Back 37

Endothelium

Front 38

This vessel is made up of endothelial cells, with no elastic or muscle tissue; exchange of cellular nutrients and metabolic end products take place here:

Back 38

Capillaries

Front 39

These vessels are large-diameter, thin walled vessels that return blood the the right atrium; low-pressure, high-volume system; contain semilunar valves:

Back 39

Veins

Front 40

Factors that affect the amount of blood in the venous system:

Back 40

-Arterial flow
-Compression of veins by skeletal muscles
-Alterations in thoracic and abdominal pressures
-Right atrial pressure

Front 41

These vessels are relatively small vessels made up of a small amount of muscle and connective tissue; collect blood from various capillary beds and channel it to the larger veins:

Back 41

Venules

Front 42

Stimulation of the beta-adrenergic receptors by the sympathetic nervous system does what to the heart?

Back 42

-Increases the HR; the speed of impulse conduction through the AV node; the force of atrial and ventricular contractions

Front 43

Stimulation by the parasympathetic nervous system does what to the heart?

Back 43

-Decreases HR by slowing the SA node rate and thus conduction through the AV node

Front 44

Stimulation of the alpha-adrenergic receptors by the sympathetic nervous system does what to blood vessels?

Back 44

Stimulates vascular smooth muscle result in vasoconstriction of the vessels (decreased stimulation causes vasodilation)

Front 45

Located in the aortic arch and carotid sinus; sensitive to stretch or pressure within the arterial system; causes decreased HR and peripheral vasodilation

Back 45

Baroreceptors

Front 46

Located in the aortic arch and carotid body; capable of initiating changes in HR and arterial pressure; responds due to decreased arterial O2 pressure, increased arterial CO2 pressure, and decreased plasma pH

Back 46

Chemoreceptors

Front 47

What 2 factors influence BP?

Back 47

-Cardiac Output (CO) and Systemic Vascular Resistance (SVR)
-BP = CO x SVR

Front 48

What is the difference between SBP and DBP?

Back 48

-Pulse Pressure

Front 49

What influences increases pulse pressure?

Back 49

-Exercise
-Atherosclerosis (due to increased SBP)

Front 50

What influences may decrease pulse pressure?

Back 50

-Hypovolemia
-Cardiac failure

Front 51

The perfusion pressure felt by organs in the body is:

Back 51

-Mean Arterial Pressure (MAP)
-must be greater than 60 to sustain vital organs

Front 52

Vibration of vessel or chest wall:

Back 52

Thrill

Front 53

Stiffness or inflexibility of vessel wall:

Back 53

Rigidity

Front 54

Auscultatory area located in the 2nd ICS to the left of the sternum:

Back 54

Pulmonic area

Front 55

Auscultatory area located in the 2nd ICS to the right of the sternum:

Back 55

Aortic area

Front 56

Auscultatory area located in the 5th left ICS close to the sternum:

Back 56

Tricuspid area

Front 57

Auscultatory area located in the left midclavicular line at the level of the 5th ICS:

Back 57

Mitral area

Front 58

Auscultatory area located at the 3rd left ICS near the sternum:

Back 58

Erb's point

Front 59

Sustained lifts of the chest wall in the precordial area that can be seen or palpated; may be caused by left ventricular hypertrophy:

Back 59

Heaves

Front 60

Lies medial to the midclavicular line in the 4th or 5th ICS; due to the pulsation of the apex of the heart:

Back 60

Point of maximal impulse or apical pulse

Front 61

Heart sound which is associated with the closure of the tricuspid and mitral (AV) valves; "lub"; signals the beginning of systole:

Back 61

First heart sound or S1

Front 62

Heart sound which is associated with the closure of the aortic and pulmonic (semilunar) valves, "dub"; signals the beginning of diastole:

Back 62

Second heart sound or S2

Front 63

Apical heart rate exceeds the peripheral pulse rate:

Back 63

Pulse deficit

Front 64

Turbulent flow sound in peripheral artery:

Back 64

Arterial bruit

Front 65

Extra heart sound, low pitched, heard in early diastole; known as ventricular gallop:

Back 65

Third heart sound or S3

Front 66

Extra heart sound, low pitched, heard in late diastole (precedes S1); known as atrial gallop:

Back 66

Fourth heart sound or S4

Front 67

Turbulent sounds occurring between normal heart sounds; characterized by loudness, pitch, shape, quality, duration; timing; graded on a 6-point scale using Roman numeral ratios:

Back 67

Murmurs

Front 68

High-pitched, scratchy sound heard during S1 and/or S2 at the apex; heard best with patient sitting and leaning forward, and at the end of expiration:

Back 68

Pericardial friction rub

Front 69

Dilated, tortuous sub-q veins most frequently found in the saphenous system:

Back 69

Varicosities or varicose veins

Front 70

More common in women and patients with a strong family hx, are probably caused by congenital weakness of the veins:

Back 70

Primary varicose veins

Front 71

Typically result from a previous DVT or another identifiable obstruction:

Back 71

Secondary varicose veins

Front 72

Smaller varicose veins that appear flat, less tortuous, and blue-green in color:

Back 72

Reticular veins

Front 73

Very small visible vessels that appear bluish-black, purple, or red:

Back 73

Telangiectasias or spider veins

Front 74

Included is: congenital weakness of the vein structure, female gender, use of hormones, increasing age, obesity, pregnancy, venous obstruction, or occupations that require prolonged standing:

Back 74

-Risks factors for developing varicosities

Front 75

As valves are stretched, venous blood flow is reversed and as back pressure increases and the calf muscle pump fails, further venous distention results:

Back 75

-Pathophysiology of varicosities

Front 76

Includes the following: discomfort varies for individuals; cosmetic disfigurement is the largest complaint; ache or pain after prolonged standing, which is relieved by walking or by elevating the limb; swelling, nocturnal leg cramps:

Back 76

Signs and Symptoms of Variscosities

Front 77

Includes the following: not usually indicated if only a cosmetic problem; sclerotherapy, laser therapy, high-intensity pulsed-light therapy, and surgery (last resort):

Back 77

Treatments of Varicosities

Front 78

Instruct pt to avoid sitting or standing for long periods of time, maintain ideal body weight, take precautions against injury to extremities, avoid wearing constrictive clothing, and participate in a daily walking activity:

Back 78

Nursing Actions for Viscosities

Front 79

Describe the 3 parts of Virchow's Triad:

Back 79

1. Venous Stasis
2. Endothelial Damage
3. Hypercoagulability of Blood

Front 80

Localized platelet aggregation and fibrin entrap RBCs, WBCs, and more platelets to form a thrombus:

Back 80

-Pathophysiology of Thrombophlebitis and DVT

Front 81

-May have a palpable, firm, sub-q cordlike vein; area surrounding the vein may be tender to the touch, reddened, and warm; mild systemic temp elevation and leukocytosis:

Back 81

-Signs and Symptoms of Superficial Thrombophlebitis

Front 82

Including the following: elevation of affected extremity, application of warm, moist heat, remove cath (if inserted), TED, mild pain relievers, NAIDs for inflammation; anticoagulant therapy is usually not indicated:

Back 82

-Treatment of Superficial Thrombophlebitis

Front 83

-May or may not have the following: unilateral leg edema, pain, warm skin, erythema, temp >100.4, tenderness upon palpation, and a positive Homan's sign:

Back 83

-Signs & Symptoms of DVT

Front 84

-early mobilization; frequent change of position in bed; TED; ICDs; elevation, anticoagulation therapy (including Coumadin, UH, LMWH), warm compression:

Back 84

-Treatment of DVT (including preventative measures)

Front 85

INR monitors what drug(s)? What is its normal and therapeutic value?

Back 85

-Monitors Coumadin
-Normal value: 0.75-1.25
-Thera: 2-3

Front 86

aPTT or activated partial thromboplastin time monitors what drug(s)? What is its normal and therapeutic value?

Back 86

-Monitors UH and Hirudin derivatives
-Normal value: 24-36 sec
-Thera: 47-70 sec

Front 87

ACT or activated clotting time monitors what drug(s)? What is its normal and therapeutic value?

Back 87

-Monitors Heparin, Hirudin derivatives, and Argatroban (Acove)
-Normal value: 80-135 sec
-Thera: 3 min

Front 88

Involves progressive narrowing and degeneration of the arteries of the neck, abdomen, and extremities; occurs at age 60-80; 2x more common

Back 88

-Peripheral Arterial Disease

Front 89

A gradual thickening of the intima and media or arteries, which leads to progressive narrowing of the vessel lumen:

Back 89

-Atherosclerosis

Front 90

Pathologic changes that occur with atherosclerosis consist of:

Back 90

-Migration and replication of smooth muscle cells
-Deposition of connective tissue
-Lymphocyte and macrophage infiltration
-Accumulation of lipids

Front 91

List the 4 most significant risk factors of PAD:

Back 91

1. Smoking
2. Hyperlipidemia
3. HTN
4. Diabetes Mellitus

Front 92

Other risk factors of PAD include:

Back 92

-Obesity, elevated triglycerides, elevated uric acid, family historym stress, sedentary lifestyle

Front 93

-Termed as hardening of the arteries
-Atherosclerosis is the major cause

Back 93

-CAD

Front 94

-Focal deposit of cholesterol and lipids primarily within the intimal wall of the artery; inflammation and endothelial injury play a central role in development; takes many years to develop and a person does not become symptomatic until the disease has advanced

Back 94

-Pathophysiology of CAD

Front 95

What are causes of arterial wall injury and inflammation?

Back 95

-Tobacco use, hyperlipidemia, HTN, diabetes, hyperhomocysteinemia, and infection which causes local inflammatory response

Front 96

This stage of CAD development is the earliest lesion; characterized by lipid-filled smooth muscle cells; yellow tinged; can be observed as early as 15 years old; believed treatment that lowers LDL can also reverse this process:

Back 96

-Fatty Streak

Front 97

This stage of development of CAD is the beginning of progressive changes in the endothelium of the arterial wall; occurs by the age of 30; appears whitish or grayish; can form on one portion of the artery or circulatory around the lumen; results in narrowing of the lumen and reduction of blood flow to distal tissues; attracts platelets and puts at risk for thrombus formation:

Back 97

-Fibrous Plaque

Front 98

This developmental stage of CAD: final stage; most dangerous; once the artery's wall is compromised, platelets accumulate in large numbers, leading to a thrombus and further narrowing or total occlusion of the artery:

Back 98

-Complicated Lesion

Front 99

Name the 4 major risk factors of development of CAD:

Back 99

1. Elevated Serum Lipids
2. Hypertension
3. Tobacco Use
4. Physical Inactivity

Front 100

At what cholesterol and fasting triglyceride value is considered elevated and a greater risk factor of CAD?

Back 100

-Serum cholesterol level of >200 mg/dl
-Fasting triglyceride level of >150 mg/dl

Front 101

-High levels of this lipoprotein is good; low levels are a risk factor of CAD; carry lipids away from arteries to the liver for metabolism; prevents lipid accumulation within arterial walls; levels can be increased by physical activity, moderate alcohol consumption, and estrogen admin

Back 101

-HDLs or High-density lipoproteins

Front 102

-Low levels of this lipoprotein is considered bad; high levels are a risk factor of CAD; contain more cholesterol than any other; have an attraction for arterial walls

Back 102

-LDLs or Low-density lipoproteins

Front 103

What is the LDL goal for persons at low risk of development of CAD? Those with a very high risk?

Back 103

-Low risk: <160 mg/dl

-Very high risk: <70 mg/dl

Front 104

Name risk factors for developing elevated serum levels:

Back 104

-Certain diseases
-Drugs
-Genetic disposition
-High alcohol consumption
-High intake of refined carbs and simple sugars
-physical inactivity

Front 105

Name:
-Normal BP level:
-Prehypertensive level:
-Stage 1 hypertension:
-Stage 2 hypertension:

Back 105

-Normal: <120/80 mmHg
-PreHTN: 120-139 mmHg/80-89 mmHg
-Stage 1: 140-159 mmHg/90-99 mmHg
-Stage 2: >160 mmHg/100 mmHg

Front 106

Name the 3 ways drug therapy works to decrease the risk of CAD complications:

Back 106

1. Restrict Lipoprotein Production
-statin drugs
2. Increase Lipoprotein Removal
-bile-acid sequestrants
3. Decrease Cholesterol Absorption
-zetia

Front 107

When the demand for myocardial O2 exceeds the ability of the coronary arteries to supply the heart with O2:

Back 107

-Myocardial Ischemia occurs

Front 108

Otherwise known as chest pain; the clinical manifestation of reversible myocardial ischemia:

Back 108

-Angina

Front 109

How quickly after coronary occlusion does the myocardium become hypoxic?

Back 109

-10 seconds

Front 110

With total occlusion, contractility ceases after several minutes; glucose and O2 are deprived for aerobic metabolism; lactic acid accumulates irritating myocardial nerve fibers which transmit a pain message to cardiac nerves and left shoulder/arm:

Back 110

-Pathophysiology of Chronic Stable Angina

Front 111

With restoration of blood flow, aerobic metabolism resumes, contractility is restored, and cellular repair begins. During ischemic conditions, cardiac cells are viable for approximately how long?

Back 111

-20 minutes

Front 112

What does PQRST stand for?

Back 112

P: Precipitating events
Q: Quality of pain
R: Radiation of pain
S: Severity of pain
T: Timing

Front 113

Describe key points of Chronic Stable Angina:

Back 113

-Described as a pressure or ache
-Rarely sharp or stabbing pain
-Usually does not change with position or breathing
-Usually lasts 3-5 minutes
-Pain at rest is unusual
-Can be controlled with meds
-Often predictable

Front 114

Refers to ischemia that occurs in the absence of an subjective symptoms; diabetics are thought to have increased prevalence:

Back 114

-Silent ischemia

Front 115

Occurs only at night but not necessarily when the person is in the recumbent position or during sleep:

Back 115

-Nocturnal Angina

Front 116

Chest pain that occurs only while the person is lying down and is usually relieved by standing or sitting:

Back 116

-Angina Decubitus

Front 117

A rare form that often occurs at rest, usually in response to spasm of a major coronary artery:

Back 117

-Prinzmetal's Angina