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HLSC 222 - Pathophysiology Across the Lifespan > Chapter 24 - Alterations in Cardiovascular Function > Flashcards

Chapter 24 - Alterations in Cardiovascular Function Flashcards

1
Q

What is a varicose vein?

A

a vein where blood has pooled, producing distended and palpable vessels

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2
Q

What 2 things cause varicose veins?

A
  1. trauma that damages valves
  2. gradual distention by gravity
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3
Q

How do vein valves get damaged?

A

increased pressure and blood volume due to the pressure of gravity

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4
Q

Which veins usually become varicose veins?

A

saphenous veins of the legs

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5
Q

Varicose veins: __________ remodel the vessel wall

A

enzymes

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6
Q

When varicose veins swell from pressure, what is pushed through the vessel wall?

A

plasma

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7
Q

Why does standing for long periods of time put one at risk for varicose veins?

A

it diminishes the action of muscle pump

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8
Q

What are 4 other risk factors for varicose veins

A

-age
-obesity
-genetics
-pregnancy
-previous leg injury

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9
Q

What is the non-invasive treatment for varicose veins?

A

-elevate legs
-compression stockings

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10
Q

What is the invasive treatment for varicose veins?

A

surgical ligation

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11
Q

What is surgical ligation?

A

tying up the blood vessel

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12
Q

What is chronic venous insufficiency?

A

inadequate venous return over an extended period

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13
Q

What are the symptoms of chronic venous insufficiency?

A

-edema of lower extremities
-hyperpigmentation of ankle and feet skin

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14
Q

Poor circulation, and thus reduced oxygen cells leads to ____________

A

necrosis

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15
Q

What is a risk of chronic venous insufficiency?

A

infection

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16
Q

reduced __________ makes surgery a risk

A

circulation

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17
Q

Venous stasis ulcers is an infection that occurs due to ______ __________ in veins

A

poor circulation

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18
Q

Venous stasis ulcers result from impaired oxygen delivery that leads to __________

A

necrosis

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19
Q

What is a thrombus?

A

a blood clot that remains attached to the vessel wall

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20
Q

What is a thromboembolism?

A

a detached thrombus

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21
Q

Why are venous thrombi more common that arterial thrombi?

A

flow and pressure are lower in veins

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22
Q

Thrombi occur more often where?

A

lower extremities

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23
Q

What is the the Virchow triad?

A

the 3 factors that promote Deep Venous Thrombosis (DVT)

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24
Q

What are the Virchow triad?

A
  1. venous stasis (immobility, age, heart failure)
  2. venous endothelial damage
  3. hyper-coagulable states
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25
Q

What is a hyper-coagulable state?

A

increased tendency of blood to thrombose

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26
Q

What causes a hyper-coagulable state?

A

-pregnancy
-oral contraceptives
-heredity

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27
Q

What causes a venous obstruction?

A

accumulation of clotting factors and platelets near a venous valve

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28
Q

With thrombus formation, _________ promotes further platelet aggregation

A

inflammation

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29
Q

Obstruction creates __________ edema and possible ulceration of limb

A

extremity

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30
Q

Ulceration of Limb

A

break on the skin surface

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31
Q

Most thrombus dissolve without treatment but others can be treated with ________________

A

anticoagulants

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32
Q

What are some examples of anticoagulants?

A

aspirin and warfarin

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33
Q

How are venous thrombi diagnosed?

A

doppler ultrasonography

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34
Q

What is a doppler ultrasound?

A

a non-invasive test that estimates blood flow through vessels by bouncing high-frequency sound waves

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35
Q

What is superior vena cava (SVC) syndrome?

A

the progressive occlusion of the superior vena cave leading to venous distention

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36
Q

Where does SVC syndrome venous distension affect?

A

upper extremities and head

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37
Q

Bronchogenic cancer is the cause of _____% of SVC syndrome cases

A

75%

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38
Q

What results from SVC syndrome?

A

-edema
-venous distension in upper extremities and face

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39
Q

Symptoms of SVC Syndrome

A

-tightness of shirt collars and necklaces
-headache
-visual disturbances

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40
Q

How is SVC syndrome diagnosed?

A

-chest x-ray
-CT
-MRI

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41
Q

What is hypertension?

A

consistent elevation of systemic arterial blood pressure

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42
Q

_______ and _______ pose risk for hypertension

A

age and diabetes

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43
Q

What two mechanisms are essential for maintaining a proper blood pressure?

A

exercise and proper nutrition

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44
Q

Primary hypertension can be essential or __________

A

idiopathic

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45
Q

95% of cases are _____________ hypertension

A

primary

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46
Q

What causes secondary hypertension?

A

a separate underlying disorder

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47
Q

___% of cases involve secondary hypertension

A

5%

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48
Q

What is malignant hypertension?

A

rapidly progressing hypertension

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49
Q

Malignant hypertension involves a systolic BP above ______ mmHg and a diastolic BP above ______ mmHg

A

180; 120

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50
Q

Malignant hypertension can lead to ________ and _________ complications

A

systemic; organ

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51
Q

Malignant hypertension is considered…

A

a medical emergency

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52
Q

What is a normal blood pressure value?

A

systolic <120 and diastolic <80

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53
Q

What is an elevated blood pressure value?

A

systolic 120-129 and diastolic <80

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54
Q

Stage 1 Hypertension value:

A

systolic 130-139 OR diastolic 80-89

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55
Q

Stage 2 Hypertension value:

A

systolic ≥140 OR diastolic ≥90

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56
Q

What are the values of a hypertensive crisis?

A

systolic >180 and/or diastolic >120

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57
Q

Primary hypertension is caused by a combination of genetic and ____________ factors

A

environmental

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58
Q

Epigenetics

A

how behaviours and environment affect gene function

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59
Q

Hypertension results from sustained peripheral ___________ and/or an increase in ________ ________

A

resistance; blood volume

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60
Q

What two primary factors contribute to primary hypertension?

A

-the sympathetic nervous system
-RAAS

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61
Q

How does increased SNS stimulation increase blood pressure?

A

increased HR, increased contractibility, systemic vasoconstriction

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62
Q

What does RAAS stand for?

A

renin-angiotensin-aldosterone system

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63
Q

How does aldosterone increase bp?

A

it increases Na+ reabsorption to increase blood volume (water follows Na+)

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64
Q

How does angiotensin II increase bp?

A

it increases vasopressin (ADH) which increases vasoconstriction

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65
Q

What is sclerosis?

A

abnormal hardening of body tissue

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66
Q

What is arteriosclerosis?

A

a generic term for vascular disease that causes thickening and inelasticity of arteries

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67
Q

Atherosclerosis is a dominant pattern of __________

A

arteriosclerosis

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68
Q

What is atherosclerosis?

A

formation of fatty plague with a core rich in lipids

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69
Q

Athera is the Greek word for ______ and it means…

A

athero; porridge

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70
Q

Treatment for hypertension begins with lifestyle modifications such as:

A

-diet
-exercise
-stopping smoking
-weight loss

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71
Q

What are two advances treatments for hypertension?

A

-diuretics
-angiotensin II blockers

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72
Q

Orthostatic hypotension is defined as a decrease in systolic bp of ___ mmHg or a decrease in diastolic BP of ___ mmHg within ___ minutes of standing

A

20; 10; 3

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73
Q

What adjustments are normally made to maintain BP when standing?

A

-baroreceptors
-vasoconstriction
-heart rate

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74
Q

What are the signs and symptoms of orthostatic hypotension?

A

-dizziness
-vision loss
-reduced brain blood flow

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75
Q

Is there a curative Tx for orthostatic hypotension?

A

no

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76
Q

What are ways to manage orthostatic hypotension?

A

-increased fluid and salt intake
-thigh high stockings

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77
Q

What is an aneurysm?

A

a localized dilation of a vessel wall

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78
Q

An aneurysm involves all ______ layers of the vessel wall

A

three

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79
Q

Aneurysms progressively _______ the vessel wall

A

weaken

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80
Q

What is the most common vessel to suffer an aneurysm?

A

aorta - a region of constant high pressure stress

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81
Q

What are 3 risk factors for aneurysm?

A

-smoking
-genetics
-diet

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82
Q

What are the 3 layers of the blood vessel from innermost to outermost?

A

tunica intima, tunica media, tunica adventita

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83
Q

What is an embolsim?

A

a vessel obstruction by an embolus

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84
Q

What is an embolus?

A

a bolus of matter circulating in the blood stream

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85
Q

An embolism can can consist of a dislodged _______, aggregation of fat/_______ cells, or foreign substance

A

thrombus; cancer

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86
Q

An embolus travels in the blood stream until it reaches…

A

a vessel through which it can’t pass

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87
Q

An embolism causes ischemia and if not resolved can lead to infarction which is…

A

ischemia resulting in necrosis

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88
Q

What is thromboangiitis obliterans?

A

inflammation of peripheral arteries

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89
Q

Thromboangiitis obliterans aka _______ disease

A

Buerger’s

90
Q

Thromboangiitis obliterans is strongly associated with ________

A

smoking

91
Q

Thromboangiitis obliterans is an ____________ disease that involves a thrombus filled with ______ cells

A

autoimmune; immune

92
Q

Thromboangiitis obliterans occludes _________ arteries

A

smallers

93
Q

What are the symptoms of Thromboangiitis obliterans?

A

-pain
-tenderness in affected areas (extremities usually)

94
Q

What are the signs of Thromboangiitis obliterans?

A

-reddish skin
-thickened and malformed nails

95
Q

Advanced Thromboangiitis obliterans can cause ________ and possible ________ may be needed

A

gangrene; amputation

96
Q

What is the treatment for Thromboangiitis obliterans?

A

stopping smoking

97
Q

_____________ is the leading cause of Coronary Artery Disease (CAD)

A

atherosclerosis

98
Q

What can cause atherosclerosis?

A

-smoking
-hypertension
-diabetes
-increased low-density lipoproteins (LDLs)
-decreased high-density lipoproteins (HDLs)
-autoimmune action

99
Q

Atherosclerosis begins with injury to the __________ cells that line the artery wall, causing them to become inflamed

A

epithelial

100
Q

Atherosclerosis: the inflamed cells express __________ molecules that bind ________ which release cytokines and enzymes to further damage the wall

A

adhesion; macrophages

101
Q

Atherosclerosis: inflammation causes ____ ______ to oxidize LDL that have accumulated in the tunica ______

A

free radicals; intima

102
Q

What is a “foam cell”?

A

a macrophage that engulfs oxidized LDLs

103
Q

What accumulates to form the fatty streak?

A

foam cells

104
Q

The fatty streak leads to __ cells being recruited in an autoimmune response to cause further damage

A

T

105
Q

Which cells release growth factors to produce collagen?

A

macrophages

106
Q

Collagen accumulation over the fatty streak forms a _______ ______

A

fibrous plague

107
Q

Protrusion of the fibrous plague from the lumen…

A

obstructs/occludes blood flow

108
Q

What is a complicated plague?

A

when the fibrous plague ruptures

109
Q

What do complicated plagues form?

A

rapid thrombus formation

110
Q

Thrombus formation from atherosclerosis can lead to ______ or ________

A

ischemia or infarction

111
Q

The ischemia and infarction from atherosclerosis causes ______ from deprived oxygen and nutrients which impairs function

A

hypoxia

112
Q

With CAD, the myocardial cells remain _______ but not properly functioning

A

alive

113
Q

What causes Acute Coronary Syndromes (ACS)?

A

persistent ischemia

114
Q

Myocardial infarction is an _____

A

ACS

115
Q

Infarction can trigger a _____ _____

A

heart attack

116
Q

What is a cardiac infarction?

A

obstruction of blood supply causing irreversible myocardial damage

117
Q

LDLs are responsible for the delivery of _________ to tissues

A

cholesterol

118
Q

A high intake of __________ and __________ fats elevates serum LDL levels

A

cholesterol; saturated

119
Q

High LDL levels causes LDL __________ into vessel walls which imitates ___________

A

migration; atherosclerosis

120
Q

HDLs are responsible for the delivery of excess cholesterol back to the ________

A

liver

121
Q

HDLs play a role in endothelial ______ which decreases _________

A

repair; thrombosis

122
Q

Have elevated HDL levels proven to prevent cv disease?

A

no

123
Q

___________ is responsible for the 2-3-fold increase in CAD risk

A

hypertension

124
Q

Hypertension causes _________ injury, which leads to atherosclerosis and myocardial hypertrophy

A

endothelial

125
Q

Myocardial hypertrophy increases the ________ demand of the heart

A

oxygen

126
Q

Smoking promotes _______ ______ generation

A

free radical

127
Q

What does nicotine stimulate that increases BP?

A

catecholamines (epi and nor-epi)

128
Q

How do catecholamines increase BP?

A

by increasing HR and inducing vasoconstriction

129
Q

CAD risk decreases when…

A

smoking stops

130
Q

Smoking is associated with ________ LDL and ___________ HDL levels

A

increased; decreased

131
Q

Abdominal obesity is the strongest risk of ______

A

CAD

132
Q

Abdominal obesity is related to __________ and ________ HDL

A

inflammation; decreased

133
Q

A sedentary lifestyle increases risk for ________ and CAD

A

obesity

134
Q

What is an atherogenic diet?

A

a diet that promotes the formation of fatty plagues in arteries

135
Q

Atherogenic diet aka “______-style Diet”

A

Western

136
Q

Which diet is most recommended for health?

A

Mediterranean

137
Q

What is a high-sensitivity C-reactive protein test (hs-CRP test)

A

a blood test that can detect very low levels of C-reactive protein

138
Q

Elevated serum hs-CRP is linked to _____

A

CAD

139
Q

What is C-reactive protein (CRP)?

A

a protein synthesized in the liver in response to inflammation in the body

140
Q

hs-CRP is used to determine risk of heart disease and ______ in people without known heart disease

A

stroke

141
Q

hs-CRP value <1 mg/L =

A

low risk of cardiovascular disease

142
Q

hs-CRP value 1-3 mg/L =

A

average risk of cardiovascular disease

143
Q

hs-CRP value >3 mg/L =

A

high risk of cardiovascular disease

144
Q

What are adipokines?

A

hormones released from adipose cells - leptin and adiponectin

145
Q

Obesity is associated with increased ___________

A

inflammation

146
Q

Obesity involves ________ leptin and _________ adiponectin

A

increased; decreased

147
Q

What does adiponectin do?

A

protect vascular endothelium and is anti-inflammatory

148
Q

When does myocardial ischemia develop?

A

when blood-borne oxygen levels aren’t meeting metabolic demands

149
Q

How does atherosclerosis cause myocardial ischemia?

A

plague ruptures and forms a thrombus which occludes blood flow

150
Q

Myocardial cells become ischemic within ___ seconds of occlusion

A

10

151
Q

Myocardial ischemia causes a shift to anaerobic respiration causing _____ _____ to accumulate and decreasing the rate of _____ re-phosphorylation

A

lactic acid; ATP

152
Q

After several minutes of myocardial ischemia, the heart loses the ability to _______

A

contract

153
Q

If perfusion is not restored within ____ seconds, myocardial infarction occurs

A

20

154
Q

Angina

A

chest pain caused by myocardial ischemia

155
Q

What is stable angina pectoris?

A

gradual narrowing and hardening of arterial walls associated with inflammation and decreased endothelial vasodilators

156
Q

With stable angina pectoris, vessels can’t response to increase demand during…

A

exercise or emotional stress

157
Q

Stable angina pectoris decreases with ______ and _______

A

rest and nitrates

158
Q

What is Prinzmetal’s angina?

A

transient angina that occurs unpredictably and often at rest/sleep

159
Q

What is the cause of Prinzmetal’s angina?

A

vasospasm of coronary arteries

160
Q

Silent ischemia involves the symptoms of fatigue and ______

A

dyspnea

161
Q

Silent ischemia can occur _______ or with ______

A

alone; angina

162
Q

Slient ischemia increases risk for a…

A

cardiac event

163
Q

Physical examination for myocardial ischemia displays:

A

-rapid pulse
-extra heart sounds

164
Q

Pulmonary congestion indicates impaired _____ ventricular function

A

left

165
Q

What is the most effective tool to detect myocardial ischemia?

A

SPECT - single-photon emission computed tomography

166
Q

What is the treatment for myocardial ischemia?

A

-diet
-exercise
-surgery: placement of coronary stent

167
Q

What is unstable angina?

A

harbinger of impending infarction - when a coronary thrombosis leads to myocardial ischemia

168
Q

Harbinger

A

announces the “coming of something”

169
Q

An acute attack of harbinger angina signals…

A

atherosclerotic plague has become unstable and infarction may soon follow

170
Q

Superficial erosion of plague leads to _________ episodes of thrombotic occlusion and vasoconstriction

A

transient

171
Q

Thrombotic occlusion from unstable angina lasts no more than ___ to ___ minutes

A

10 to 20

172
Q

Unstable angina symptom:

A

Prinzmetal angina increasing in severity

173
Q

How is unstable angina diagnosed?

A

ECG during attack or hs-cTnt

174
Q

How is unstable angina seen on an ECG?

A

-ST depression
-T inversion
-ST elevation

175
Q

High-sensitivity Cardiac Troponin test identifies tiny amounts of enzymes released from damaged _______

A

myocytes

176
Q

What is the treatment for unstable angina?

A

immediate hospitalization

177
Q

Myocardial infarction can be non-______ or _______

A

STEMI

178
Q

Non-STEMI Myocardial Infarction

A

persistent occlusion leads to infarction of myocardium closest to endocardium

179
Q

STEMI Myocardial Infarction

A

continued occlusion leads to infarction from endocardium to pericardium

180
Q

Name layers of the heart from innermost to outermost:

A

endocardium, myocardium, pericardium

181
Q

How long does oxygen depletion occur after onset of myocardial infarction?

A

10 seconds

182
Q

After 10 seconds, affected myocardium becomes ________ and cooler

A

cyanotic

183
Q

anaerobic metabolism leads to ___ and ______ _____ accumulation and reduced ATP production

A

H+ and lactic acid

184
Q

Why do electrolyte disturbances affect the hearts ability to contract?

A

myocardial cells need K+ and calcium

185
Q

_______ cells accompany electrolyte disturbances with O2 deprivation and contribute to further tissue damage

A

immune

186
Q

Cardiac cells can withstand ischemic conditions for ____ mins before irreversible damage

A

20

187
Q

What are the symptoms of a myocardial infarction?

A

acute, sudden, severe chest pain

188
Q

How is a myocardial infarction diagnosed?

A

hs-cTnT

189
Q

Heart failure definition: when the heart is unable to generate adequate cardiac output causing inadequate ________ of tissues and/or increased ________ filling pressure of the ____ ventricle, so that pulmonary capillary pressures are increased.

A

perfusion; diastolic; left

190
Q

Heart failure affects 10% of individuals older than ___

A

65

191
Q

What is the most common reason for hospital admission in people over 65?

A

heart failure

192
Q

Most heart failure is due to the dysfunction of the ______ ventricle

A

left

193
Q

Left Ventricular Failure with Reduced Ejection Factor definition: left ventricle ejection fraction less than ___% normal which results in the inability of the heart to ________ tissue

A

40%; perfuse

194
Q

CO = ____ x ____

A

SV x HR

195
Q

What are the determinants of SV?

A

-contractility
-preload
-afterload

196
Q

Ventricular remodelling results in ________ of the left ventricle

A

dilation

197
Q

What causes ventricular remodelling?

A

progressive myocyte contractile dysfunction

198
Q

Ventricular remodelling results in reduced _____ _____ and increased left ventricular ___-_______ _______

A

stroke volume; end-diastolic volume

199
Q

The main causes of myocardial dysfunction are:

A

-myocardial infarction
-ischemic heart disease
-hypertension

200
Q

Reduced perfusion due to ↓CO and ↓ systemic BP results in ↑ _______ activity

A

sympathetic

201
Q

Increased sympathetic activity means…

A

-increased catecholamine secretion
-increased vasoconstriction

202
Q

Decreased perfusion of kidneys activates the _____ to increase __________ and blood volume

A

RAAS; vasoconstriction

203
Q

The overall result of L ventricular failure with reduced ejection factor is…

A

-↑ cardiac after load
-↑ BP
-↑ HR
and thus ventricular remodelling

204
Q

↓ myocyte function = increased _______ (due to decreased contractility)

A

preload

205
Q

What are the effects of increased preload?

A

-stretching of myocardium
-sarcomere dysfunction

206
Q

What are the effects of increased afterload?

A

-systemic hypertension
-myocardial hypertrophy (remodelling)
-increased O2 demand

207
Q

The changes from increased afterload are called…

A

hypertensive hypertrophic cardiomyopathy

208
Q

____% of heart failure patients have previous hypertension

A

75%

209
Q

Hypertrophy

A

increase in size of cells

210
Q

↓ in CO = ↓ in ______ perfusion

A

renal

211
Q

With LVF w/ reduced ejection factor, ________ continue to detect a decreased blood pressure so catecholamine release and vasoconstriction are still increased

A

baroreceptors

212
Q

What pharmacological interventions are needed for LVF w/ reduced ejection factor?

A

inhibition of aspects of RAAS and SNS

213
Q

What is left ventricular failure with preserved ejection factor?

A

pulmonary congestion despite normal stroke volume and cardiac output

214
Q

What is the prevalence of LVFpEF in the population?

A

1-5%

215
Q

LVFpEF is caused by abnormal diastolic _______ so a normal LVEDV results in an _________ left-ventricular end-diastolic pressure (LVEDP)

A

relaxation; increased (aka normal amount of blood returning to heart results in an increased ventricular pressure)

216
Q

How does LVFpEF result in pulmonary edema and right ventricular hypertrophy?

A

the pressure is reflected back into pulmonary circulation

217
Q

How is LVFpEF diagnosed?

A

-dyspnea on exertion
-fatigue
-evidence of pulmonary edema

218
Q

What is right ventricular failure?

A

inability of the right ventricle to provide adequate blood flow into pulmonary circulation at a normal venous pressure

219
Q

Right ventricular failure can be caused by ______________ that reflects pressure back into the pulmonary system and right ventricle

A

left ventricular failure

220
Q

Why does the right ventricle dilate and fail from increased pressure?

A

it is poorly prepared

221
Q

Systemic hypertension leads to…

A

peripheral edema

222
Q

Cor Pulmonale

A

when a lung issue causes your right ventricle to fail

HLSC 222 - Pathophysiology Across the Lifespan (17 decks)

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