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SMIT Pathology > Chapter 4 Cardiovascular Function > Flashcards

Chapter 4 Cardiovascular Function Flashcards

1
Q

Functions of the cardiovascular system

A

Delivers vital oxygen and nutrients to cells
Removes waste products
Transports hormones

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2
Q

Systemic branch of the cardiovascular system

A

Carries blood throughout the body to meet the body’s needs and remove waste products
Includes arteries, veins, and capillaries
Works with the lymphatic system

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3
Q

Pulmonary branch of the cardiovascular system

A

Carries blood to and from the lungs for gas exchange

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4
Q

Pericardium

A

Surrounds the heart to provide protection and support

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5
Q

Myocardium

A

muscle portion of the organ

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6
Q

Endocardium

A

Inner structures, including the valves

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7
Q

Function of atria

A

receiving chambers

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8
Q

Function of ventricles

A

pumping chambers

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9
Q

Blood flow through the heart

A

Blood from the systemic circulation enters from the superior vena cava and the inferior vena cava

Blood empties directly into the right atrium
From the right atrium, blood travels through the tricuspid valve to the right ventricle

The right ventricle pumps blood through the pulmonic valve to the pulmonary arteries

The pulmonary arteries carry blood to the lungs for gas exchange

Blood from the pulmonary circulation enters from the pulmonary veins

Blood empties directly into the left atrium

Blood leaves the left atrium through the mitral valve to the left ventricle

The left ventricle then pumps blood through the aortic valve to the aorta

From the aorta the blood is carried the rest of the body

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10
Q

Excitability

A

ability of the cells to respond to electrical impulses

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11
Q

Conductivity

A

ability of cells to conduct electrical impulses

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12
Q

Automaticity

A

ability to generate an impulse to contract with no external nerve stimulus

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13
Q

What is the rate of impulses generated by SA node?

A

60 - 100 bpm

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14
Q

What is the rate of impulses initiated by AV node?

A

40 - 60 bpm

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15
Q

Depolarization

A

Increase in electrical charge
Accomplished through cellular ion exchange
Generates cardiac contraction

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16
Q

Repolarization

A

Cellular recovery
Ions returning to the cell membrane in preparation for depolarization

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17
Q

Chronotropic effects

A

rate of contraction

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18
Q

Inotropic effects

A

strength of contraction

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19
Q

Blood pressure

A

Force that blood exerts on the walls of blood vessels

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20
Q

Systolic

A

top number; cardiac work phase

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21
Q

Diastolic

A

bottom number; cardiac rest phase

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22
Q

Influences on blood pressure

A

Cardiac Output

Peripheral vascular resistance (PVR)

Afterload

Preload

Hormones

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23
Q

Afterload

A

pressure needed to eject the blood

Blood viscosity
PVR

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24
Q

Preload

A

amount of blood returning

Blood volume
Venous return

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25
Q

Hormones affecting the blood pressure

A

Antidiuretic hormone (ADH)
Renin-angiotensin-aldosterone system

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26
Q

Arteries

A

Carry blood away

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27
Q

Veins

A

Carry blood back

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28
Q

Capillaries

A

site of exchange

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29
Q

Three layers of blood vessels

A

Tunica intima – inner layer
Tunica media – middle muscular layer
Tunica adventitia – outer elastic layer

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30
Q

Features of lymphatic system

A

Works to return excess interstitial fluid (lymph) to the circulation

Plays a role in immunity

Includes lymph nodes, the spleen, the thymus, and the tonsils

Excessive amount of lymph -> edema

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31
Q

Pericarditis

A

Inflammation of the pericardium

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32
Q

Pericardial effusion

A

Inflammatory process, fluid shifts from the capillaries to the space between the sac and the heart

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33
Q

Cardiac tamponade

A

the fluid accumulates in the pericardial cavity to the point that it compresses the heart

This compression prevents the heart from stretching and filling during diastole, resulting in decreased cardiac output

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34
Q

Constrictive pericarditis

A

Loss of elasticity - the pericardium becomes thick and fibrous from the chronic inflammation and adheres to the heart

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35
Q

Clinical manifestations of pericarditis

A

Pericardial friction rub (grating sound heard when breath is held)
Sharp, sudden, severe chest pain that increases with deep inspiration and decreases when sitting up and leaning forward
Dyspnea
Tachycardia
Edema
Flulike symptoms

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36
Q

Infective endocarditis

A

An infection of the endocardium (inner layers of the heart) or heart valves.

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37
Q

Etiology of Infective endocarditis

A

Commonly caused by Streptococcus and Staphylococcus infections

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38
Q

Pathogenesis of infective endocarditis

A

Endothelial damage -> Attracts platelets -> Thrombus

Vegetation forms on internal structures and creates small thrombi

Microemboli occur as they are dislodged

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39
Q

Risk factors of Infective endocarditis

A

intravenous drug use, valvular disorders, prosthetic heart valves, rheumatic heart disease, coarctation of the aorta, congenital heart defects, and Marfan syndrome

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40
Q

Clinical manifestations of Infective endocarditis

A

flulike symptoms, embolization, heart murmur, conjunctival petechiae, splinter hemorrhages under the nails, hematuria, and Osler’s nodes

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41
Q

Myocarditis

A

Inflammation of the myocardium

Uncommon

Organisms, blood cells, toxins, and immune substances invade and damage the muscle

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42
Q

Complications associated with myocarditis

A

heart failure, cardiomyopathy, dysrhythmias, and thrombus formation

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43
Q

Clinical manifestations of myocarditis

A

May be asymptomatic

Include: flulike symptoms, dyspnea, dysrhythmias, palpitations, tachycardia, heart murmurs, chest discomfort, and cardiac enlargement

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44
Q

Valvular Disorders

A

Disrupt blood flow through the heart

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45
Q

Stenosis - narrowing - Valvular disorders

A

Less blood can flow through the valve
Causes decreased cardiac output, increased cardiac workload, and hypertrophy

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46
Q

Regurgitation - insufficient closure - Valvular disorders

A

Blood flows in both directions through the valve
Causes decreased cardiac output, increased cardiac workload, hypertrophy, and dilation

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47
Q

Causes of Valvular Disorders

A

congenital defects, infective endocarditis, rheumatic fever, myocardial infarction, cardiomyopathy, and heart failure

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48
Q

Clinical manifestations

A

Vary depending on valve involved
Reflect alteration in blood flow through the heart

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49
Q

Cardiomyopathy

A

Conditions that weaken and enlarge the myocardium

Classified into three groups—
1. Dilated cardiomyopathy
2. Hypertrophic cardiomyopathy
3. Restrictive cardiomyopathy

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50
Q

Dilated cardiomyopathy

A

Most common type – affects systolic function

Risk higher with advancing age and African American men

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51
Q

Causes of Dilated Cardiomyopathy

A

Mostly idiopathic.

Other causes: chemotherapy, alcoholism, cocaine abuse, pregnancy, infections, thyrotoxicosis, diabetes mellitus, neuromuscular diseases, hypertension, coronary artery disease, and hypersensitivity to medications

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52
Q

Clinical manifestations of Dilated Cardiomyopathy

A

Appear as compensatory mechanisms fail

Includes: dyspnea, fatigue, nonproductive cough, orthopnea, paroxysmal nocturnal dyspnea, dysrhythmias, angina, dizziness, activity intolerance, blood pressure changes, tachycardia, murmurs, abnormal lung sounds, tachypnea, peripheral edema, ascites, weak pulses, cool, pale extremities, poor capillary refill, hepatomegaly, and jugular vein distension

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53
Q

Hypertrophic Cardiomyopathy

A

Affects systolic and diastolic function.

More common in men and those who are sedentary

Risk higher with hypertension, obstructive valvular disease, and thyroid disease

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54
Q

Hypertrophic cardiomyopathy is a common cause of

A

sudden cardiac death in young people, especially young athletes.

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55
Q

Pathogenesis of Hypertrophic cardiomyopathy

A

Stiff ventricle wall -> decreased ventricular filling -> decreased cardiac output -> increased atrial and pulmonary pressures

56
Q

Clinical manifestations of Hypertrophic cardiomyopathy

A

dyspnea on exertion, fatigue, syncope, orthopnea, angina, activity intolerance, dysrhythmias, left ventricular failure, and myocardial infarction

57
Q

Restrictive Cardiomyopathy

A

Least common of the cardiomyopathies.

Characterized by rigidity of the ventricles, leading to diastolic dysfunction.

58
Q

Causes of Restrictive cardiomyopathy

A

amyloidosis, hemochromatosis, radiation exposure to the chest, connective tissue diseases, myocardial infarction, sarcoidosis, and cardiac neoplasms

59
Q

Clinical manifestations of Restrictive cardiomyopathy

A

Many cases are asymptomatic

Include: fatigue, dyspnea, orthopnea, abnormal lung sounds, angina, hepatomegaly, jugular vein distension, ascites, murmurs, peripheral cyanosis, and pallor

60
Q

Electrical Alterations

A

Normal electric conduction - sinus rhythm

Deviations - dysrhythmias or arrhythmias.

Classified by origin
- Supraventricular rhythms
- Ventricular rhythms

Can affect cardiac output and blood pressure

61
Q

Causes of Electrical Alterations

A

acid-base imbalances, hypoxia, congenital heart defects, connective tissue disorders, degeneration of conductive tissues, drug toxicity, electrolyte imbalances, stress, myocardial hypertrophy, and myocardial ischemia or infarction

62
Q

Clinical manifestations of Electrical Alterations

A

May include: palpitations, fluttering sensation, skipped beats, fatigue, confusion, syncope, dyspnea, and abnormal heart rate

63
Q

Congestive Heart Failure

A

Inadequate pumping

Leads to decreased cardiac output, increased preload, and increased afterload

64
Q

In congestive heart failure, what are the activated compensatory mechanisms?

A

Activation of the sympathetic nervous system

Activation of the renin-angiotensin-aldosterone system

Ventricular hypertrophy

65
Q

Types of Heart Failure

A

Systolic dysfunction - Decreased contractility
Diastolic dysfunction - Decreased filling
Mixed dysfunction - Both

66
Q

Clinical manifestations of Heart failure

A

Depend on type - Fluctuates in severity

Appear as compensatory mechanisms fail

Includes: indications of systemic and pulmonary fluid congestion

67
Q

Aneurysms

A

Weakening of the wall of an artery

Can occur in any artery

Common in the abdominal aorta, thoracic aorta, and the cerebral, femoral, and popliteal arteries

Can rupture – exsanguination

68
Q

Risk factors of aneurysms

A

congenital defect, atherosclerosis, hypertension, dyslipidemia, diabetes mellitus, tobacco, advanced age, trauma, and infection

69
Q

True aneurysms

A

affect all three vessel layers – (intima, media, adventitia)

70
Q

Saccular aneurysm

A

bulge on the side

71
Q

Fusiform aneurysm

A

occurs the entire circumference

72
Q

False aneurysm

A

does not affect all three layers of the vessel

73
Q

Dissecting aneurysms

A

occurs in the inner layers

74
Q

Clinical manifestations of Aneurysms

A

Depend on location and size
May be asymptomatic
May include: pulsating mass, pain, respiratory difficulty (dyspnea, cough), and neurologic decline (confusion, lethargy)

75
Q

Dyslipidemia/Hyperlipidemia

A

High levels of lipids in the blood

76
Q

Classifications of Dyslipidemia/Hyperlipidemia

A

Classified based on density, which is based on the amount of triglycerides (low density) and protein (high density)

Very-low density lipoproteins
Low density lipoproteins – AKA “bad” cholesterol
High density lipoproteins – AKA “good” cholesterol

77
Q

Clinical manifestations of Dyslipidemia/Hyperlipidemia

A

asymptomatic until it develops into other diseases

78
Q

Atherosclerosis

A

Chronic inflammatory disease characterized by thickening and hardening of the arterial wall.

79
Q

Pathogenesis of Atherosclerosis

A

Inflammatory process is triggered by a vessel wall injury

Lesions develop on the vessel wall and calcify over time

Leads to vessel obstruction, platelet aggregation, and vasoconstriction

80
Q

Complications of atherosclerosis

A

peripheral vascular disease, coronary artery disease, thrombi, hypertension, and stroke

81
Q

Clinical manifestations of atherosclerosis

A

asymptomatic until complications develop

82
Q

Peripheral Vascular Disease

A

Narrowing of the peripheral vessels

83
Q

Etiology of Peripheral Vascular Disease

A

atherosclerosis, thrombus, inflammation, and vasospasms

84
Q

Thromboangiitis obliterans

A

an inflammatory condition of the arteries

85
Q

Raynaud’s disease

A

vasospasms of arteries, usually in the hands, because of sympathetic stimulation

86
Q

Raynaud’s phenomenon

A

associated with an autoimmune condition

87
Q

Clinical manifestations of Peripheral Vascular Disease

A

pain, intermittent claudication, numbness, burning, non-healing wounds, skin color changes, hair loss, and impotency

88
Q

Coronary Artery Disease

A

Atherosclerotic changes of the coronary arteries

Impairs myocardial tissue perfusion

89
Q

Angina

A

chest pain resulting from myocardium ischemia

90
Q

Infarction

A

necrotic damage to the myocardium

91
Q

Etiology of Coronary Artery Disease

A

atherosclerosis, vasospasms, thrombus, and cardiomyopathy

92
Q

Pathogenesis of Coronary Artery Disease

A

Atherosclerosis in coronary arteries -> Decreased blood flow -> Decreased Oxygen to heart muscles -> chest pain

93
Q

Stable angina

A

goes away with demand reduction

94
Q

Unstable angina

A

increased intensity or frequency, does not go away with demand reduction, or occurs at rest

95
Q

Complications associated with Coronary Artery Disease

A

myocardial infarction, heart failure, dysrhythmias, and sudden death

96
Q

Clinical manifestations of CAD

A

angina, indigestion-like sensation, nausea, vomiting, clammy extremities, diaphoresis, and fatigue

97
Q

Thrombus

A

Stationary blood clot

98
Q

Virchow’s triad

A

endothelial injury, sluggish blood flow, and increased coagulation

99
Q

Emboli

A

traveling body

100
Q

Prevention from thrombus

A

increasing mobility, hydration, antiembolism hose, sequential compression devices, antiplatelet agents, and anticoagulants

101
Q

Varicose veins

A

Engorged veins resulting from valve incompetency

Most common in the legs

May also occur as esophageal varices and hemorrhoids

102
Q

Pathogenesis of Varicose Veins

A

Increased venous pressure and blood pooling -> Enlarged veins and incompetent valves -> Increased capillary pressure -> Fluid leak

103
Q

Complications associated with Varicose Veins

A

cause stasis pigmentation (brown skin discoloration), subcutaneous induration (thick, hardened skin), dermatitis (skin inflammation), and thrombophlebitis (vein inflammation resulting from a thrombus)

104
Q

Risk factors of Varicose Veins

A

genetic predisposition, pregnancy, obesity, prolonged sitting or standing, alcohol abuse and liver disorders (esophageal varices), and constipation (hemorrhoids)

105
Q

Clinical manifestations

A

Irregular, purplish, bulging veins
Pedal edema
Fatigue
Aching in the legs
Shiny, pigmented, hairless skin on the legs and feet
Skin ulcer formation

106
Q

Lymphedema

A

Swelling due to a lymph obstruction

107
Q

Primary lymphedema

A

Rare, usually congenital

108
Q

Secondary lymphedema

A

Causes: surgery, radiation, cancer, infection, and injury

109
Q

Manifestations of lymphedema

A

hyperpigmentation, ulcerations, and thickening of the skin

110
Q

Myocardial infarction

A

Death of the myocardium

Coronary artery blood flow is blocked due to atherosclerosis, thrombus, or vasospasms

111
Q

Clinical manifestations of Myocardial Infarction

A

Some are asymptomatic – “Silent” MI

Includes: angina, fatigue, nausea, vomiting, shortness of breath, diaphoresis, indigestion, elevation in cardiac markers, electrocardiogram changes

112
Q

Complications associated with MI

A

heart failure, dysrhythmias, cardiac shock, thrombosis, and death

113
Q

Diagnosis of MI

A

history, physical examination, electrocardiogram, cardiac markers, stress testing, nuclear imaging, and angiography

114
Q

Treatment of MI

A

Varies depending on timing of treatment

Immediately: Morphine, Oxygen, Nitrate, Aspirin; may also administer thrombolytics

Post-MI: similar to those for atherosclerosis

115
Q

Hypertension

A

Prolonged elevation in blood pressure

In hypertension, the heart is working harder than normal to pump the blood to all the parts of the body.

116
Q

Risk factors of Hypertension

A

advancing age, ethnicity, family history, being overweight or obese, physical inactive, tobacco use, high-sodium diet, low-potassium diet, high vitamin D intake, excessive alcohol intake, stress, and other chronic conditions

117
Q

Primary hypertension

A

Most common form
Develops gradually over time

118
Q

Secondary hypertension

A

Tends to be more sudden and severe
Causes: renal disease, adrenal gland tumors, certain congenital heart defects, certain medications, and illegal drugs

119
Q

Malignant hypertension

A

Intensified form
Does not respond well to treatment

120
Q

Manifestations of hypertension

A

“Silent killer”
Include: fatigue, headache, malaise, and dizziness

121
Q

Complications of Hypertension

A

atherosclerosis, aneurysms, heart failure, stroke, hypertensive crisis, renal damage, vision loss, metabolic syndrome, memory problems

122
Q

Pregnancy-induced hypertension

A

Hypertension first seen in pregnancy

123
Q

Risk factors of Pregnancy-induced hypertension

A

history of pregnancy-induced hypertension, renal disease, diabetes mellitus, multiple fetuses, and maternal age less than 20 years or greater than 40 years

124
Q

Complications of Pregnancy-induced hypertension

A

seizures, miscarriages, poor fetal development, and placental abruption

125
Q

Treatment of Hypertension

A

bed rest and magnesium sulfate

126
Q

Shock

A

Decreased blood volume or circulatory stagnation resulting in inadequate tissue and organ perfusion

127
Q

Compensatory stage of Shock

A

Sympathetic nervous system and renin-angiotensin-aldosterone system are activated

128
Q

Progressive stage of Shock

A

Compensatory mechanisms fail
Tissues become hypoxic, cells switch to anaerobic metabolism, lactic acid builds up, and metabolic acidosis develops

129
Q

Irreversible stage of Shock

A

Organ damage occurs

130
Q

Distributive shock

A

results from excessive vasodilation and the impaired distribution of blood flow.

131
Q

Neurogenic shock

A

Loss of vascular sympathetic tone and autonomic function lead to massive vasodilatation

132
Q

Septic shock

A

Bacterial endotoxins activate an immune reaction

133
Q

Anaphylactic shock

A

Excessive allergic reaction

134
Q

Cardiogenic shock

A

Left ventricle cannot maintain adequate cardiac output

135
Q

Hypovolemic shock

A

Venous return reduces because of external blood volume losses

136
Q

Complications of Shock

A

acute respiratory distress syndrome, renal failure, disseminated intravascular coagulation, cerebral hypoxia, and death

137
Q

Clinical Manifestations of Shock

A

Varies depending on type

Include: thirst, tachycardia, restlessness, irritability, tachypnea progressing to Cheyne-Stokes respiration, cool and pale skin, hypotension, cyanosis, and decreasing urinary output

SMIT Pathology (4 decks)

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