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
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
3
Q
Pulmonary branch of the cardiovascular system
A
Carries blood to and from the lungs for gas exchange
4
Q
Pericardium
A
Surrounds the heart to provide protection and support
5
Q
Myocardium
A
muscle portion of the organ
6
Q
Endocardium
A
Inner structures, including the valves
7
Q
Function of atria
A
receiving chambers
8
Q
Function of ventricles
A
pumping chambers
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
10
Q
Excitability
A
ability of the cells to respond to electrical impulses
11
Q
Conductivity
A
ability of cells to conduct electrical impulses
12
Q
Automaticity
A
ability to generate an impulse to contract with no external nerve stimulus
13
Q
What is the rate of impulses generated by SA node?
A
60 - 100 bpm
14
Q
What is the rate of impulses initiated by AV node?
A
40 - 60 bpm
15
Q
Depolarization
A
Increase in electrical charge
Accomplished through cellular ion exchange
Generates cardiac contraction
16
Q
Repolarization
A
Cellular recovery
Ions returning to the cell membrane in preparation for depolarization
17
Q
Chronotropic effects
A
rate of contraction
18
Q
Inotropic effects
A
strength of contraction
19
Q
Blood pressure
A
Force that blood exerts on the walls of blood vessels
20
Q
Systolic
A
top number; cardiac work phase
21
Q
Diastolic
A
bottom number; cardiac rest phase
22
Q
Influences on blood pressure
A
Cardiac Output
Peripheral vascular resistance (PVR)
Afterload
Preload
Hormones
23
Q
Afterload
A
pressure needed to eject the blood
Blood viscosity
PVR
24
Q
Preload
A
amount of blood returning
Blood volume
Venous return
25
Hormones affecting the blood pressure
Antidiuretic hormone (ADH)
Renin-angiotensin-aldosterone system
26
Arteries
Carry blood away
27
Veins
Carry blood back
28
Capillaries
site of exchange
29
Three layers of blood vessels
Tunica intima – inner layer
Tunica media – middle muscular layer
Tunica adventitia – outer elastic layer
30
Features of lymphatic system
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
31
Pericarditis
Inflammation of the pericardium
32
Pericardial effusion
Inflammatory process, fluid shifts from the capillaries to the space between the sac and the heart
33
Cardiac tamponade
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
34
Constrictive pericarditis
Loss of elasticity - the pericardium becomes thick and fibrous from the chronic inflammation and adheres to the heart
35
Clinical manifestations of pericarditis
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
36
Infective endocarditis
An infection of the endocardium (inner layers of the heart) or heart valves.
37
Etiology of Infective endocarditis
Commonly caused by Streptococcus and Staphylococcus infections
38
Pathogenesis of infective endocarditis
Endothelial damage -> Attracts platelets -> Thrombus
Vegetation forms on internal structures and creates small thrombi
Microemboli occur as they are dislodged
39
Risk factors of Infective endocarditis
intravenous drug use, valvular disorders, prosthetic heart valves, rheumatic heart disease, coarctation of the aorta, congenital heart defects, and Marfan syndrome
40
Clinical manifestations of Infective endocarditis
flulike symptoms, embolization, heart murmur, conjunctival petechiae, splinter hemorrhages under the nails, hematuria, and Osler’s nodes
41
Myocarditis
Inflammation of the myocardium
Uncommon
Organisms, blood cells, toxins, and immune substances invade and damage the muscle
42
Complications associated with myocarditis
heart failure, cardiomyopathy, dysrhythmias, and thrombus formation
43
Clinical manifestations of myocarditis
May be asymptomatic
Include: flulike symptoms, dyspnea, dysrhythmias, palpitations, tachycardia, heart murmurs, chest discomfort, and cardiac enlargement
44
Valvular Disorders
Disrupt blood flow through the heart
45
Stenosis - narrowing - Valvular disorders
Less blood can flow through the valve
Causes decreased cardiac output, increased cardiac workload, and hypertrophy
46
Regurgitation - insufficient closure - Valvular disorders
Blood flows in both directions through the valve
Causes decreased cardiac output, increased cardiac workload, hypertrophy, and dilation
47
Causes of Valvular Disorders
congenital defects, infective endocarditis, rheumatic fever, myocardial infarction, cardiomyopathy, and heart failure
48
Clinical manifestations
Vary depending on valve involved
Reflect alteration in blood flow through the heart
49
Cardiomyopathy
Conditions that weaken and enlarge the myocardium
Classified into three groups—
1. Dilated cardiomyopathy
2. Hypertrophic cardiomyopathy
3. Restrictive cardiomyopathy
50
Dilated cardiomyopathy
Most common type – affects systolic function
Risk higher with advancing age and African American men
51
Causes of Dilated Cardiomyopathy
Mostly idiopathic.
Other causes: chemotherapy, alcoholism, cocaine abuse, pregnancy, infections, thyrotoxicosis, diabetes mellitus, neuromuscular diseases, hypertension, coronary artery disease, and hypersensitivity to medications
52
Clinical manifestations of Dilated Cardiomyopathy
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
53
Hypertrophic Cardiomyopathy
Affects systolic and diastolic function.
More common in men and those who are sedentary
Risk higher with hypertension, obstructive valvular disease, and thyroid disease
54
Hypertrophic cardiomyopathy is a common cause of
sudden cardiac death in young people, especially young athletes.
55
Pathogenesis of Hypertrophic cardiomyopathy
Stiff ventricle wall -> decreased ventricular filling -> decreased cardiac output -> increased atrial and pulmonary pressures
56
Clinical manifestations of Hypertrophic cardiomyopathy
dyspnea on exertion, fatigue, syncope, orthopnea, angina, activity intolerance, dysrhythmias, left ventricular failure, and myocardial infarction
57
Restrictive Cardiomyopathy
Least common of the cardiomyopathies.
Characterized by rigidity of the ventricles, leading to diastolic dysfunction.
58
Causes of Restrictive cardiomyopathy
amyloidosis, hemochromatosis, radiation exposure to the chest, connective tissue diseases, myocardial infarction, sarcoidosis, and cardiac neoplasms
59
Clinical manifestations of Restrictive cardiomyopathy
Many cases are asymptomatic
Include: fatigue, dyspnea, orthopnea, abnormal lung sounds, angina, hepatomegaly, jugular vein distension, ascites, murmurs, peripheral cyanosis, and pallor
60
Electrical Alterations
Normal electric conduction - sinus rhythm
Deviations - dysrhythmias or arrhythmias.
Classified by origin
- Supraventricular rhythms
- Ventricular rhythms
Can affect cardiac output and blood pressure
61
Causes of Electrical Alterations
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
Clinical manifestations of Electrical Alterations
May include: palpitations, fluttering sensation, skipped beats, fatigue, confusion, syncope, dyspnea, and abnormal heart rate
63
Congestive Heart Failure
Inadequate pumping
Leads to decreased cardiac output, increased preload, and increased afterload
64
In congestive heart failure, what are the activated compensatory mechanisms?
Activation of the sympathetic nervous system
Activation of the renin-angiotensin-aldosterone system
Ventricular hypertrophy
65
Types of Heart Failure
Systolic dysfunction - Decreased contractility
Diastolic dysfunction - Decreased filling
Mixed dysfunction - Both
66
Clinical manifestations of Heart failure
Depend on type - Fluctuates in severity
Appear as compensatory mechanisms fail
Includes: indications of systemic and pulmonary fluid congestion
67
Aneurysms
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
Risk factors of aneurysms
congenital defect, atherosclerosis, hypertension, dyslipidemia, diabetes mellitus, tobacco, advanced age, trauma, and infection
69
True aneurysms
affect all three vessel layers – (intima, media, adventitia)
70
Saccular aneurysm
bulge on the side
71
Fusiform aneurysm
occurs the entire circumference
72
False aneurysm
does not affect all three layers of the vessel
73
Dissecting aneurysms
occurs in the inner layers
74
Clinical manifestations of Aneurysms
Depend on location and size
May be asymptomatic
May include: pulsating mass, pain, respiratory difficulty (dyspnea, cough), and neurologic decline (confusion, lethargy)
75
Dyslipidemia/Hyperlipidemia
High levels of lipids in the blood
76
Classifications of Dyslipidemia/Hyperlipidemia
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
Clinical manifestations of Dyslipidemia/Hyperlipidemia
asymptomatic until it develops into other diseases
78
Atherosclerosis
Chronic inflammatory disease characterized by thickening and hardening of the arterial wall.
79
Pathogenesis of Atherosclerosis
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
Complications of atherosclerosis
peripheral vascular disease, coronary artery disease, thrombi, hypertension, and stroke
81
Clinical manifestations of atherosclerosis
asymptomatic until complications develop
82
Peripheral Vascular Disease
Narrowing of the peripheral vessels
83
Etiology of Peripheral Vascular Disease
atherosclerosis, thrombus, inflammation, and vasospasms
84
Thromboangiitis obliterans
an inflammatory condition of the arteries
85
Raynaud’s disease
vasospasms of arteries, usually in the hands, because of sympathetic stimulation
86
Raynaud’s phenomenon
associated with an autoimmune condition
87
Clinical manifestations of Peripheral Vascular Disease
pain, intermittent claudication, numbness, burning, non-healing wounds, skin color changes, hair loss, and impotency
88
Coronary Artery Disease
Atherosclerotic changes of the coronary arteries
Impairs myocardial tissue perfusion
89
Angina
chest pain resulting from myocardium ischemia
90
Infarction
necrotic damage to the myocardium
91
Etiology of Coronary Artery Disease
atherosclerosis, vasospasms, thrombus, and cardiomyopathy
92
Pathogenesis of Coronary Artery Disease
Atherosclerosis in coronary arteries -> Decreased blood flow -> Decreased Oxygen to heart muscles -> chest pain
93
Stable angina
goes away with demand reduction
94
Unstable angina
increased intensity or frequency, does not go away with demand reduction, or occurs at rest
95
Complications associated with Coronary Artery Disease
myocardial infarction, heart failure, dysrhythmias, and sudden death
96
Clinical manifestations of CAD
angina, indigestion-like sensation, nausea, vomiting, clammy extremities, diaphoresis, and fatigue
97
Thrombus
Stationary blood clot
98
Virchow's triad
endothelial injury, sluggish blood flow, and increased coagulation
99
Emboli
traveling body
100
Prevention from thrombus
increasing mobility, hydration, antiembolism hose, sequential compression devices, antiplatelet agents, and anticoagulants
101
Varicose veins
Engorged veins resulting from valve incompetency
Most common in the legs
May also occur as esophageal varices and hemorrhoids
102
Pathogenesis of Varicose Veins
Increased venous pressure and blood pooling -> Enlarged veins and incompetent valves -> Increased capillary pressure -> Fluid leak
103
Complications associated with Varicose Veins
cause stasis pigmentation (brown skin discoloration), subcutaneous induration (thick, hardened skin), dermatitis (skin inflammation), and thrombophlebitis (vein inflammation resulting from a thrombus)
104
Risk factors of Varicose Veins
genetic predisposition, pregnancy, obesity, prolonged sitting or standing, alcohol abuse and liver disorders (esophageal varices), and constipation (hemorrhoids)
105
Clinical manifestations
Irregular, purplish, bulging veins
Pedal edema
Fatigue
Aching in the legs
Shiny, pigmented, hairless skin on the legs and feet
Skin ulcer formation
106
Lymphedema
Swelling due to a lymph obstruction
107
Primary lymphedema
Rare, usually congenital
108
Secondary lymphedema
Causes: surgery, radiation, cancer, infection, and injury
109
Manifestations of lymphedema
hyperpigmentation, ulcerations, and thickening of the skin
110
Myocardial infarction
Death of the myocardium
Coronary artery blood flow is blocked due to atherosclerosis, thrombus, or vasospasms
111
Clinical manifestations of Myocardial Infarction
Some are asymptomatic – “Silent” MI
Includes: angina, fatigue, nausea, vomiting, shortness of breath, diaphoresis, indigestion, elevation in cardiac markers, electrocardiogram changes
112
Complications associated with MI
heart failure, dysrhythmias, cardiac shock, thrombosis, and death
113
Diagnosis of MI
history, physical examination, electrocardiogram, cardiac markers, stress testing, nuclear imaging, and angiography
114
Treatment of MI
Varies depending on timing of treatment
Immediately: Morphine, Oxygen, Nitrate, Aspirin; may also administer thrombolytics
Post-MI: similar to those for atherosclerosis
115
Hypertension
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
Risk factors of Hypertension
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
Primary hypertension
Most common form
Develops gradually over time
118
Secondary hypertension
Tends to be more sudden and severe
Causes: renal disease, adrenal gland tumors, certain congenital heart defects, certain medications, and illegal drugs
119
Malignant hypertension
Intensified form
Does not respond well to treatment
120
Manifestations of hypertension
“Silent killer”
Include: fatigue, headache, malaise, and dizziness
121
Complications of Hypertension
atherosclerosis, aneurysms, heart failure, stroke, hypertensive crisis, renal damage, vision loss, metabolic syndrome, memory problems
122
Pregnancy-induced hypertension
Hypertension first seen in pregnancy
123
Risk factors of Pregnancy-induced hypertension
history of pregnancy-induced hypertension, renal disease, diabetes mellitus, multiple fetuses, and maternal age less than 20 years or greater than 40 years
124
Complications of Pregnancy-induced hypertension
seizures, miscarriages, poor fetal development, and placental abruption
125
Treatment of Hypertension
bed rest and magnesium sulfate
126
Shock
Decreased blood volume or circulatory stagnation resulting in inadequate tissue and organ perfusion
127
Compensatory stage of Shock
Sympathetic nervous system and renin-angiotensin-aldosterone system are activated
128
Progressive stage of Shock
Compensatory mechanisms fail
Tissues become hypoxic, cells switch to anaerobic metabolism, lactic acid builds up, and metabolic acidosis develops
129
Irreversible stage of Shock
Organ damage occurs
130
Distributive shock
results from excessive vasodilation and the impaired distribution of blood flow.
131
Neurogenic shock
Loss of vascular sympathetic tone and autonomic function lead to massive vasodilatation
132
Septic shock
Bacterial endotoxins activate an immune reaction
133
Anaphylactic shock
Excessive allergic reaction
134
Cardiogenic shock
Left ventricle cannot maintain adequate cardiac output
135
Hypovolemic shock
Venous return reduces because of external blood volume losses
136
Complications of Shock
acute respiratory distress syndrome, renal failure, disseminated intravascular coagulation, cerebral hypoxia, and death
137
Clinical Manifestations of Shock
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
