Chapter 24 - Alteration In CV Function Flashcards
(182 cards)
1
Q
Varicose veins
A
Veins where blood has pooled producing distended and palpable vessels
2
Q
Cause of Varicose veins
A
Trauma that damages valves or gradual distension caused by action of gravity
3
Q
Valve damage due to
A
Increase pressure and volume of blood under pressure of gravity
4
Q
Varicose veins typically involve what veins of the leg
A
Saphenous veins of legs
5
Q
Pathophysiology of varicose veins
A
Enzymes remodel vessel wall, and veins swells with increased pressure and pressure pushes plasma through vessel wall
6
Q
Risk factors for varicose veins
A
-standing for long periods which diminishes action of muscle pump
-age, obesity, genetics, pregnancy, previous leg injury
7
Q
Varicose vein TX
A
-elevated legs, compression stockings
Invasive TX: surgical ligation -> tying up blood vessel
8
Q
Chronic venous insufficiency
A
Inadequate venous return over ext3ended period
9
Q
Symptoms of Chronic venous insufficiency
A
-edema of lower extremities
-hyperpigmentation of ankle and feet skin
-circulation sluggish, reduced oxygen to cells causing necrosis
-surgery
10
Q
Venous statis ulcers
A
Infection occurs because of poor circulation in veins and impairs delivery of oxygen causing necrosis
11
Q
Thrombus
A
Blood clot that remains attached to vessel wall
12
Q
Thromboembolism
A
A detachedthrombus
13
Q
Venous thrombi are more common than
A
Arterial thrombi as flow and pressure are lower in veins
-also occurs more often in lower extremity
14
Q
The virchow triad
A
Three factors that promote deep venous thrombosis
1. Venous stasis (immboity, age, heart failure)
2. Venous endothelial damage
3. Hypercoagulable states (inc tendency of blood to thromboses)
15
Q
Hypercoagulable states are caused by
A
Pregnancy, oral contraceptives, heredity
16
Q
Pathophysiology of thrombus formation in veins
A
-Accumulation of clotting factors and platelets near a venous valve cause venous obstruction
-inflammation promote further planet aggregation causing pain and redness
17
Q
Thrombus obstruction creates extremity edema causing
A
Ulceration of limb (break on surface)
18
Q
TX for thrombus formation in veins
A
Most thrombus dissolve without treatment
-anticoagulants (aspirin, warfarin)
19
Q
Diagnosis for thrombus formation in veins
A
Doppler ultrasonography
20
Q
Doppler ultrasonography
A
Non invasive test that can be used to estimate blood flow through blood vessels by bouncing high frequency sound waves
21
Q
Superior vena cava syndrome
A
Progressive occlusion of Superior vena cava leading to venous distension to upper extremities and head
22
Q
Causes for Superior vena cava syndrome
A
Bronchogenic cancer
-75% of cases
-ontological emergency
23
Q
Pathophysiology of Superior vena cava syndrome
A
Lung bronchi abuts Superior vena cava syndrome = bronchi cancer puts pressure on SRV
24
Q
Result of Superior vena cava syndrome
A
Edema and venous distension in upper extremities and face
25
Effect of Superior vena cava syndrome
Tightness of shirt collars, necklaces, headache, visual disturbances
26
Diagnosis of Superior vena cava syndrome
Chest, X-ray, CT, MRI
27
Hypertension
Consistent elevation of systemic arterial blood pressure
28
Risk of hypertension
Increases with age, higher in diabetes
29
Maintenance of proper BP
Exercise and proper nutrition
30
Percentage of primary hypertension vs secondary hypertension
95% of cases and 5% of cases
31
Malignant hypertension
Rapidly progressive hypertension
S: >180, D: >120
-system and organ complications, can be considered a medical emergency
32
Normal BP
Less than 120/less than 80
33
Elevated BP
120-129/less than 80
34
High blood pressure (stage 1)
130-139/80-89
35
High blood pressure stage 2
140+/90+
36
Hypertensive crisis
180+/120+
37
Factors associated with primary hypertension
No specific cause
-genetic and environmental factors
-epigenetic changes
38
Epigentic
How behaviours and environment affect gene function
39
Hypertension results form
Sustained inc in peripheral resistance, inc in blood volume
40
Two primary factors of primary hypertension
1. Sympathetic ns
2. RAAS
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SNS and primary hypertension
Inc SNS will cause INC HR, cardiac contractility, systemic vasoconstriction = rise in BP
42
RAAS
Renin angiotesin, angiotesnin II, aldosterone pathways
43
RAAS increases in (aldosterone vs angiotensin II)
1. Aldosterone = inc Na reabsorption from kidney, inc blood volume, inc BP
2. Angiotensin II = inc vasopressin which inc vasoconstriction and inc BP
44
Arteriosclerosis
A: Genetic term for vascular disease in which causes thickening an inelasticity of arteries
S: hardening of body tissue
45
Atherosclerosis
Dominant pattern of arteriosclerosis
-formation of fatty plague with core rich in lipids
46
Athero
From Greek word athera meaning porridge
47
TX for hypertension
Begin with lifestyle modifications: diet, exercise, stopping, smoking, loosing weight
Advanced: diuretics, angiotensin II blockers
48
What is orthostatic hypotension
Decrease in systolic BP of 20 mmHg or a decrease in diastolic BP of 10 mmHg within three minutes of standing
-mechanical dysfunction
49
Normally what happens during standing
Baroreceptors, vasoconstriction and heart rate adjusts to maintain normal BP
50
Signs and symptoms of orthostatic hypotension
Dizziness, loss of vision, reduced brain blood flow
51
Treatment for othrostatic hypotension
No curative treatment
-inc fluid and salt intake, wearing thigh high stockings
52
Aneurysm
Localized dilation of vessel wall
53
What layers of the arterial wall does an Aneurysm involve
All three layers, causing weakening
54
What is the most common site of an Aneurysm
Aorta
-constant high pressure stress
55
Risk factors of Aneurysm
Smoking, genetics, diet
56
What are the three CV vessel layers
Tunica adventitia, tunica media, tunica intima
57
Embolism
Vessel obstruction by an embolus (bolus of matter circulating in blood stream)
58
An embolism consists of
A dislodged thrombus, aggregating of fat or cancer cells, and foreign substances
59
Embolus travels in blood stream until it reaches
A vessel through which it can’t pass
60
Embolism causes
Ischemia (restricted blood supply)
-continual obstruction can cause infarction (ischmeia resulting in necrosis)
61
Thromboangiitis obliterans (buergers disease)
Inflammation of peripheral artery
-strongly associated with smoking
-autoimmune disease
62
How is Thromboangiitis obliterans (buergers disease), an autoimmune disease
Thrombus is filled with immune cells, causing an occlusion of smaller arteries
63
S/s of Thromboangiitis obliterans (buergers disease)
Symptoms: pain and tenderness in affected area
Signs: reddish skin, thickened and malformed nails
64
TX for Thromboangiitis obliterans (buergers disease)
Stopping smoking
-if you don’t stop amputation is likely required
65
Atherosclerosis
Formation of fatty plague with a core rich in lipid
66
What is the leading cause of CAD
Atherosclerosis
67
Atherosclerosis is caused by
Smoking, hypertension, diabetes, inc LDL, dec HDL, autoimmune
68
Pathophysiology of Atherosclerosis
Begins with injury to epithelial cells lining artery wall
-injured cells become inflamed
-inflamed cells express adhesions molecules that bind macrophages
-bound macrophages releases cytokines damaging vessel wall
-cause free radicals to oxidize LDL
-macrophages engulf oxidized LDL
-macrophages are now considered foam cell
-foam cells accumulatte and form fatty streak
-fatty streak results in recruitment of T cells
-macrophages release growth factors producing collagen
-collagen accumulates over fatty streak forming a fibrous plague
-fibrous plague protrudes into lumen and obstructs blood flow
-this fibrous plague may rupture (complicated plagues)
-producing rapid thrombus formation
-ishcemia or infarction
69
How does Atherosclerosis being?
Injury to epithelial cell lining artery wall
70
Inflammation caused free radicals to do what?
Oxidize LDL
71
Foam cell
Macrophages that have engulfed oxidized LDL
-form fatty streak
72
Fatty streak results in
Recruitment of T cells
-more damaged to vessel wall
73
Fibrous plague
Collagen accumulation from growth factors
-obstructs and occludes blood flow
74
Complicated plagues
Fibrous plagues that have ruptures
-rapid thrombus formation
75
Coronary heart disease is usually caused by
Atherosclerosis
-plague build up diminishing blood supply to cardiac muscle cells
76
Results of Coronary heart disease
Myocardial ischemia and infarction deprives heart muscle of blood borne oxygen and nutrients
-impairs heart pumping ability
77
Myocardial cells remain ___ but are not
Alive, not functioning properly
78
Persistent ischemia caused
Acute coronary syndromes
-including myocardial infarction
79
Infarction potentially triggers a
Heart attack
80
Cardiac infarction
Obstruction of blood supply causing irreversible myocardial damage
81
Dyslipidemia has a link between
Abnormal lipoprotein levels and CAD
82
Lipoproteins
High density lipoproteins (HDL) and low density lipoproteins (LDL)
83
What is responsible for delivery of cholesterol to tissues?
LDL
84
What is responsible for delivery of excess cholesterol back to liver?
HDL
85
LDL
High intake of cholesterol and saturated fats will elevate levels
-can cause LDL migration into vessel walls = atherosclerosis
86
HDL
Plays a role in endothelial repair and decreases thrombosis
-elevated levels of HDL has not proven to prevent CV disease
87
What is responsible for 2-3 fold inc in CAD risk
Hypertension
88
Hypertension causes
Endothelial injury, myocardial hypertrophy which inc heart oxygen demand
89
Why is cigarette smoking a risk for CAD
-free radical generation
-nicotine simulates catecholamines and inc HR, BP and vasoconstriction
-inc LDL, Dec HDL
90
Why is obesity a risk for CAD
Abdominal obesity
-inflammation and Dec HDL
-strongest risk of CAD
91
Why is sedentary lifestyle a risk for CAD
Not only inc risk of obesity but on its own inc risk of CAD
92
Why is a Atherogenic diet a risk for CAD
Western style diet
-promotes fatty plagues in arteries
93
Diet most recommended for health
Mediterranean diet
94
Hs-CRP test
High sensitivity C reactive protein test
-can detect very low levels of C reactive protein
-measures general levels of inflammation in body
95
Elevated serum hs-CRP is correlated to
Increased CAD risk
96
CRP
Protein synthesized in liver in response to inc in inflammation in body
97
Hs-CRP test is used to determine
Heart disease risk and stroke in people without known heart disease
98
Hs-CRP value: <1 mg/L
Low risk
99
Hs-CRP value: 1-3mg/L
Average risk
100
Hs-CRP value: >3 mg/L
High risk
101
Adipokines
Hormones released from adipose cells, two of which are lepton and adiponectin
102
Obesity =
-inc inflammation
-inc leptin
-Dec adiponectin
103
Adiponectin
Protects vascular endothelium and is ant-inflammatory
104
Myocardial ischemia develops when
Blood borne oxygen is insufficient to meet myocardial metabolic demands
105
Common cause of myocardial ischemia
Atherosclerosis in coronary circulation, causing plague rupture = thrombus formation, occlusion and myocardial ischemia
106
Myocardial cells become ischemia within ___ seconds of occlusion
10
107
Shifts toward anaerobic causes
Lactic acid accumulation, decreased rate of ATP re-phosphorylation
108
After several minutes
Heart loses ability to contract
109
If perfusion is not restored…
Myocardial infarction occurs within 20 minutes
110
Angina
Chest pain caused by myocardial ischemia
111
Stable angina pectoris
Gradual narrowing and hardening of arterial walls associated with inflammation and decreased endothelial vasodilators
112
Stable angina pectoris: affected vessels
Cannot respond to inc myocardial demand during exercise or emotional stress
-causing angina
113
Stable angina pectoris: angina decreases with
Rest and nitrates
114
Prinzmetals angina
Transient angina that occurs unpredictably and often at rest/sleep
115
Cause of Prinzmetals angina
Vasospasm risk of cardiac event
116
Silent ischemia
Occurs alone or with angina
-inc risk of cardiac event
117
Abnormal symptoms of Silent ischemia
Fatigue, dyspnea (bad breathing)
118
Evaluation for myocardial ischemia
Physical examination displays rapid pulse and extra heart sounds
119
Pulmonary congestion indicates impaired
Left ventricle function
120
Single photon emission computed tomography (SPECT) is the most
Effective tool
121
TX for myocardial ischemia
Diet and exercise
-surgery in coronary vessels dilated and placement of coronary stent
122
harbinger
Impending infarction
-Announces the coming of something
123
Unstable angina: acute attack signals
Atherosclerotic plague has become unstable, and infarction may soon follow
124
Unstable angina: superficial erosion of plague leads to
Transient episodes of thrombotic occlusion and vasoconstriction
-occlusions lasts no more than 10-20 minutes
125
Unstable angina: distinct symptom
Prinzmetal angina increasing in severity
126
Diagnosis of Unstable angina
-ECG during attack = ST depression, T wave inversion, ST segment elevation
-hs-cTnt = high sensitivity cardiac troponin T can identify tiny amounts of enzymes released from damaged myocytes
127
TX for Unstable angina
Immediate hospitalization
128
Clinically, MI is categorized as
Non-stemi or stemi
129
Unstable angina
Coronary thrombosis leads to myocardial ischemia
130
NON STEMI
Persistent occlusion leads to infarction of myocardium closest to endocardium
131
STEMI
Continued occlusion leads to infarction from endocardium to pericardium
132
Oxygen depletion in 10 seconds then…
After 10 seconds affected myocardium becomes cyanotic and cooler
133
Aerobic metabolism stops and
ATP generation stops due to anaerobic metabolism
-causes H+ and lactic acid to accumulate
-reduced ATP
134
Electrolyte disturbances
Loss of K and calcium from cells
-myocardial cells lose contractiability
-diminished ability of heart to contact
135
Infiltration of immune cells causes
Further tissue damage
136
Cardiac cells can withstand ischemia conditions for
20 minutes before irreversible damage `
137
Manifestations of myocardial infarction
Acute, severe chest pain
138
Diagnosis of myocardial infarction
Hs-cTnT
139
Photo on slide 20
140
Heart failure
Inadequate perfusion of tissues or inc diastolic filing pressure of left ventricle
-or both in which pulmonary capillary pressures are increased
141
Special thing to remember about heart failure
Left ventricle dysfunction will play back to pulmonary problems
142
Heart failure affects ___ of individuals older than 65 yoa
10%
143
Most common reason for hospital admission in >65 YOA
Heart failure
144
Most HF causes are due to
Dysfunction of left ventricle
145
Left ventricular failure with reduced ejection factor
Left ventricle election fraction less than 40% normal which results in inability of heart to perfuse tissue
146
CO =
SV x HR
147
Determinants of SV
Contractility, preload, afterload
148
Ventricular remodeling
Disruption of normal myocardial function
149
Ventricular remodeling results in
Dilation of left ventricle
150
Cause of ventricular remodeling
Progressive myocyte contractile dysfunction
151
Result of myocyte contractile dysfunction
Reduced stroke volume
-left ventricle end diastolic volume increases
152
Main causes of myocardial dysfunction
1. Myocardial infarction
2. Ischemic heart diseases
3. Hypertension
153
Decreased cardiac output and decreased systemic blood pressure =
Reduced perfusion of tissues
154
Results of reduced perfusion of tissues
Increased sympathetic activit
Causing:
-inc secretion of catecholamines
-inc vasoconstriction
155
Decreased perfusion of kidneys results in
RAAS activation and increased vasoconstriction and blood volume
156
Overall result of Left ventricular failure with reduced ejection factor
-inc cardiac afterload
-inc bp
-inc hr
-ventricular remodeling
157
Ventricular remodeling causes
Progressive myocyte remodeling over time
-dysfunction
158
Decreased myocyte function =
Decreased contractility which results in increased preload
159
Effects of increased preload
-stretching of myocardium and sarcomere dysfunction
-further dysfunction in myocardial function
160
Effects of increased afterload
results of systemic hypertension
-vasoconstriction and inc blood volume
161
___% of HF cases have previous hypertension
75
162
Increased afterload =
Myocardial hypertrophy
-myocardial remodeling
163
Hypertrophy =
Inc myocardial oxygen demand
164
Changes are referred to as
Hypertensive hypertrophic cardiomyopathy
165
Hypertrophic/hypertrophy
Increase in size of cells
166
As CO decreases
Renal perfusion is reduced
167
Results of renal perfusion
Further activation of RAAS pathway = continual increases in vasoconstriction and blood volume
168
Baroreceptors continue to detect
Decreased blood pressure which results in increased catecholamines release and inc vasoconstriction
169
Both activation of RAAS and Baroreceptors result in
Continued inc in both preload and afterload
170
Pharmacology
Inhibition of various aspects of RAAS and SNS
171
Left ventricular failure with preserved ejection factor
Defunded as pulmonary congestion despite normal stroke volume and cardiac output
172
Left ventricular failure with preserved ejection factor prevalence in population between
1-5%
173
Cause of Left ventricular failure with preserved ejection factor
Abnormal diastolic relaxation such that a normal left ventricle volume results in an inc left ventricle end diastolic pressure
174
Normal amount of blood returning to the heart results in
An increased ventricle pressure
175
This pressure is reflected back into pulmonary circulation and results in
Pulmonary edema and right ventricular hypertrophy
176
Diagnosis of Left ventricular failure with preserved ejection factor
-dyspnea on exertion
-fatigue
-evidence of pulmonary edema
177
Right ventricular failure
Inability of right ventricle to provide adequate blood flow into pulmonary circulation at a normal venous pressure
178
Cause of Right ventricular failure
Left ventricle failure = pressure reflected back into pulmonary system = pressure further reflected back into right ventricle
179
Right ventricle is poorly prepared for inc afterload and will
Dilate and fail
180
Result of Right ventricular failure
Systemic hypertension = peripheral edema
181
Right ventricular failure is referred to as
Cor pulmonale
182
Vide on slide 35
