Exam 4 Flashcards
1
Q
what is the goal of the circulatory system
A
-transport oxygen and nutrients
-removal of metabolic waste products within the body
2
Q
right ventricle pumps blood to the
A
lungs
3
Q
O2 intake and release of CO2 occurs in the
A
pulmonary vasculature
4
Q
left ventricle pumps oxygenated blood
A
systemically
5
Q
nutrients are absorbed into the blood as it moves through the
A
GI tract
6
Q
wastes are carried to the kindeys/lungs/liver for
A
elimination
7
Q
systemic circuit
A
-right ventricle from heart to lungs
-through pulmonic circulation
-now oxygenated from lungs to heart through left atrium
-through left ventricle
-from heart to body tissues and systemic circulation
-from body tissues to heart through right atrium
-and in the right ventricle again
8
Q
aorta, arteries and arterioles principle tissue is
A
smooth muscle
9
Q
capillaries are made of
A
single layer of endothelial cells
-exchange fluid to interstitial space
10
Q
role of the lymphatic system
A
reabsorbs fluid that leaks out of vascular network and returns to general circulation
-vessels are deep in connective tissue
11
Q
arteries three layer structure
A
-tunica intima
-tunica media
-tunica adventitia (externa)
12
Q
tunica intima layer of artery function and structure
A
-endothelial cells (living and active)
-direct contact with blood
-smooth, no blockages
-helps with clotting and collateral circulation
13
Q
tunica media layer of artery structure and function
A
-smooth muscle and elastin
-constricts and dilates
-sensitive stimulation from ANS
14
Q
tunica adventitia (externa) layer of artery structure and function
A
-supportive connective tissue
15
Q
calcium channel blockers (CCB) block
A
vasoconstriction and treat hypertension
16
Q
endothelium
A
innermost lining of blood vessels and arteries
-inside tunica intima
17
Q
people with dysfunctional endothelium have what 4 diseases and what activity that can lead to dysfunctional endothelium
A
-coronary artery disease
-diabetes
-hypertension
-hypercholesterolemia
-smokers
18
Q
lipid effect of blood composition on arteries and endothelium
A
-cholesterol (lipid not dissolved) and triglycerides (excess calories) carried by lipoproteins
19
Q
low density (LDL) effect on arteries
A
bad!
-deposited on artery walls
-areas of endothelial injury
20
Q
high density (HDL) effects on arteries
A
good!
-gathers excess LDL and takes to liver to get rid
-excreted from the body
21
Q
glucose effect of blood composition on arteries and endothelium and what can these effects lead to
A
-harms endothelial lining leading to plaque formation (atherosclerosis)
-vasoconstricts (MI and strokes)
22
Q
nicotine effect of blood composition on arteries and endothelium
A
-vasoconstrictor
-sympathetic nervous system
23
Q
hyperlipidemia etiology and what can it lead to
A
elevated levels of lipids: cholesterol (LDL and HDL) and triglycerides
-leads to atherosclerosis!
24
Q
what are some saturated fats that negatively contribute to hyperlipidemia
A
solid forms of animal fat: meat, eggs, cheese, butter, dairy products
25
name some unsaturated fats that can help with hyperlipidemia
liquid forms of fat: olive oil, peanut oil, canola oil, sesame and corn safflower oils, fish oil, margarine
26
List 7 hyperlipidemia risk factors
-family history
-smoking increases LDL and decreases HDL
-diabetes
-hypothyroidism
-dietary excess of calories, saturated fats, trans fats and cholesterol
-low physical activity
-obesity
27
list 6 effects of smoking on the body
-injures endothelium
-increased risk for thrombus formation
-vasospasm
-increased platelet aggregation (clots)
-increases HR, BP, O2 demand
-increased risk for coronary heart disease
28
why can hyperlipidemia be hard to catch and list 3 clinical manifestations
-silent disorder
-Xanthoma and Xanthelasma (big dots on eyes, slide 16)
-arcus senilis (yellow circle in eyes)
-metabolic syndrome
29
how do we diagnose hyperlipidemia
-history
-physical examination
-blood samples of lipoproteins, cholesterol, triglycerides
30
total cholesterol normal value
less than 200 mg/dL!
31
LDL cholesterol normal value
less than 100 mg/dL!
32
HDL cholesterol normal value
above 60 mg/dL is cardioprotective!
-less than 40 is major risk for heart disease !
33
triglycerides normal value
less than 150 mg/dL!
34
list 6 treatments for hyperlipidemia
-lifestyle changes
-drugs reducing triglycerides and cholesterol (fish oils, fibrates, statins)
-balloon or laser angioplasty
-stent
-CABG: coronary artery bypass graft
-peripheral arterial bypass
35
arterial blood pressure is produced by the force of
left ventricular contraction overcoming the resistance of the aorta to open the aortic valve
36
stroke volume
volume of blood leaving the heart with each contraction
37
peripheral vascular resistance (PVR)
-resistance to ejection
-degree of vessel compliance
38
vasoconstriction does what to peripheral vascular resistance
increases PVR
39
too much peripheral vascular resistance causes
pathological cardiac hypertrophy which is not good
40
what is the formula for cardiac output (CO)
stroke volume (volume of blood leaving heart with each contraction) x heart rate
-blood flow in arterial system
41
normal cardiac output
5 L/min
42
stroke volume and heart rate have an opposing relationship in the context of homeostasis meaning
-decreased stroke volume, increased heart rate
-increased stroke volume, decreased heart rate
43
formula for blood pressure
cardiac output x peripheral vascular resistance
44
how to determine MAP for blood pressures
systolic blood pressure + (2x diastolic blood pressure) divided by 3
45
What does systolic blood pressure represent and what is the normal value
cardiac contraction
-blood ejected from chamber
-lower than 120 mmHg
46
What does the diastolic blood pressure represent
cardiac relaxation
-end of contraction- filling
47
What is a normal left ventricle stroke volume
70 mL
48
difference between systolic and diastolic BP is called
pulse pressure
49
what is orthostatic hypotension and how do we quantify it
decreased BP when position is changed quickly to upright
-drop in SBP greater than or equal to 20
-drop in DBP greater than or equal to 10
50
List 6 causes of orthostatic hypotension
-reduced blood volume
-vasovagal response
-drug induced
-aging
-prolonged bed rest
-ANS disorders
51
List 4 clinical manifestations of orthostatic hypotension
-dizziness
-blurred vision
-fainting (syncope)
-injury from falls
52
orthostatic hypotension treatment
-move slowly
-avoid excessive vasodilation
-TED hose
53
renin angiotensin aldosterone system (RAAS) with BP regulation
-made and controlled in kidneys
-release stimulated by decrease in BP or volume
-end result of system is increased BP!
54
renin forms
angiotensin I
55
angiotensin converting enzyme (ACE) causes
angiotensin I conversion to angiotensin II in the lungs
56
angiotensin II is
potent vasoconstrictor and stimulated release of aldosterone
57
aldosterone increases
Na reabsorption in the kidneys and increased H2O
58
release of renin occurs when theres
excess sympathetic stimulation, decreased BP, decreased extracellular volume
59
ACE inhibitor
-pril
stop angiotensin I from turning into angiotensin II
60
how does antidiuretic hormone (ADH) relate to BP regulation
acts on nephron to increase water reabsorption
-increasing blood volume and BP
61
fluid volume with BP regulation
-increased ECF increases CO
-increased CO and increased volume increased PVR
-increased PVR increases BP
62
normal blood pressure for adults
-less than 120 mm Hg systolic
-less than 80 mmHg diastolic
63
hypertension diagnosis
-systolic BP > 130
-diastolic BP > 80
64
primary hypertension
-risk factors
-no known cause
65
secondary hypertension
clearly a side effect of another systemic disorder (a disease)
66
compare non modifiable to modifiable risk factors for primary hypertension
-non modifiable: increasing age, family history, african american, diabetes
-modifiable: obesity, dietary factors, tobacco, alchohol
67
List 6 causes of secondary hypertension
-pregnancy
-renal causes
-cardiovascular
-endocrine
-drugs
-neurologic
68
hypertension pathophysiology
high resistance against left ventricle
-damages endothelial artery lining
-susceptible to ischemia, infarction and HF
69
hypertension clinical manifestations
-"silent"
-displaced apical pulse
-aortic bruits
-lower extremity pulses, color, temp and sensation
70
hypertension measurement
-direct: arterial line
-indirect: mercury sphygmomanometer!
71
primary hypertension treatment
angiotensin converting enzyme inhibitor (ACEI)
-angiotensin receptor blocker (ARB)
-calcium channel blockers
-diuretics
72
primary hypertension lifestyle alterations
DASH diet
-low sodium and low fat food
73
primary hypertension stress reduction and physical activity
-yoga
-exercise 30 mins a day
74
primary hypertension smoking cessation
-nicotine raises BP
-increases resistance to flow
-free radicals
75
secondary hypertension damage to heart and arteries
-coarctation of arteries
-vasculitis
76
secondary hypertension damage to kidneys
-chronic kidney disease
-urinary tract obstruction
77
secondary hypertension damage to brain
-brain tumor
-intracranial hypertension
78
secondary hypertension damage to eyes
hypertensive retinopathy
79
hypertensive emergency
-diastolic greater than 120
-hospitalization
-sustained organ damage
80
hypertensive urgency
-diastolic greater than 120
-treated slower with oral medications
81
atherosclerosis non modifiable risk factors
-more males than females
-more african americans than caucasian americans
82
list 5 atherosclerosis modifiable risk factors
-excess saturated fat, cholesterol and salt
-obesity
-tobacco, alcohol and high stress
-hypertension
-diabetes mellitus
83
atherosclerosis etiology
-injury to endothelial lining
-hyperlipidemia is condition that causes atherosclerosis
84
atherosclerosis pathophysiology
-damage to endothelium with inflammation and increase vessel permeability
-thickening and luminal narrowing
-plaques develop and can rupture
85
atherosclerosis clinical manifestations
-gradual process with no symptoms till organ dysfunction
-on exam hear bruits
86
what 4 ways can we get an atherosclerosis diagnosis
-lipid profile
-inflammation causes elevated C-reactive protein
-cardiac cath
-CT scan
87
atherosclerosis treatment
-lifestyle changes (same as hyperlipidemia)
-drugs reducing triglycerides and cholesterol (same as hyperlipidemia)
-surgical options
-angioplasty
88
peripheral arterial disease (PAD) etiology
atherosclerosis involving peripheral vascular system
-disease of superficial vessels, usually legs-femoral artery
89
peripheral arterial disease (PAD) pathophysiology
-reduced arterial flow
-develops gradual over time
-leads to ischemia
90
List 7 peripheral arterial disease (PAD) clinical manifestations
-dependent rubor!
-elevated pallor!
-cool
-dry, thin, glossy legs
-diminished or absent pulses
-arterial ulcer
-intermittent claudication!
91
peripheral arterial disease (PAD) diagnosis
ankle brachial index less than 1
92
what is a peripheral arterial disease (PAD) ulcer
-painful
-pale, grey
-well defined edges
93
peripheral arterial disease (PAD) treatment
-prevention: exercise, weight control, control blood sugar
-thrombolytic agents
-bypass grafts and stents in legs
94
aneurysm etiology/pathophysiology
atherosclerosis/hypertension damages arterial lining
-arterial wall deteriorates till it bulges out and wall weakens collecting blood
95
aneurysm risk factors
atherosclerosis, hypertension, smoking
96
aneurysm clinical manifestations
-abdominal: flank or back pain, N&V, dont palpate pulsations
-cerebral: silent, "worst headache of my life"
-may hear bruit
97
aneurysm diagnosis
-usually silent till rupture
-ultrasound
-contrast CT
-MRI
98
aneurysm treatment
-AAA: assess progression and potential for rupture
-surgery if >4.5cm
-endovascular repair surgery
99
what is an aortic dissection and what causes it
arterial layer tear in lining between tunica media and intima
-caused by genetics, hypertension, atherosclerosis
100
list 4 aortic dissection clinical manifestations
-sudden
-pain in chest or back
-ripping or tearing sound
-hypertension difference between arms maybe
101
raynauds disease etiology
vasospasm from vasoconstriction of the arterioles in the digits
102
raynauds disease risk factors
-most common in women
-precipitated by cold or emotional stress!
103
list 4 raynauds disease clinical manifestations
-pain
-color change pattern: white to blue to red!
-throbbing
-paresthesia
104
what are 3 treatments for raynaud's disease
-calcium channel blockers vasodilate
-protect from cold
-decrease stress and no smoking
105
Buerger disease pathophysiology
rare inflammatory condition causing thrombus formation affecting small and medium sized arteries and veins
106
Buerger disease risk factor
smoking!
107
what is the function of the heard in the cardiovascular system
produces driving force propelling blood through vessels of circulatory system
108
heart circulation
health assessment quizlet!
109
acute coronary syndrome
-myocardial infarction
-unstable angina
110
myocardial infarction
-plaque rupture and thrombus formation
-complete occlusion! resulting in necrosis
-with or without ST segment elevation
111
what is unstable angina
-plaque rupture and thrombus formation
-partial occlusion or clot resolution!
-no ST segment elevation
112
what is stable angina and what causes it
predictable and consistent pain that occurs on exertion and is relieved by rest and/or nitroglycerin
-from narrowing and stiffening of coronary vessels!
113
cause for alarm with stable angina
patient takes 3 nitroglycerin tablets within a 10 min period without chest pain relief: assume MI!
114
what is prinxmetals (variant) angina and what does it respond to
coronary vasospasms
-unrelated to increased O2 demand
-unpredictable and responds to calcium channel blockers
115
unstable angina (acute coronary syndrome) etiology
emergency
-myocardial ischemia!
-heart muscle needs more circulation to supply cells with oxygen
116
unstable angina (acute coronary syndrome) pathophysiology
-atherosclerosis
-thrombus
-50-70% blockage
-anemia
117
unstable angina (acute coronary syndrome) clinical presentation
-sudden pain!
-pressure, choking, squeezing
-pain may radiate to epigastric region, jaw, neck, arm
118
unstable angina (acute coronary syndrome) diagnosis
-BP
-lipid profile
-thallium stress test specific for angina
-similar findings to pt with artherosclerosis
119
unstable angina (acute coronary syndrome) treatment
-prevent MI!
-oxygen
-nitrates (vasodilator), be careful with viagra because also a vasodilator
120
acute myocardial infarction (MI) etiology
prolonged or total disruption of blood flow to myocardium
-important factors: location occlusion, length of time, collateral circulation
-ATP depletion
121
what changes after MI
-area becomes pale
-necrotic tissue leaves weak area susceptible to rupture!
122
myocardial infarction clinical manifestations
-severe crushing, excruciating chest pain
-may radiate to jaw, shoulder or back
-lasts more than 25 mins
-not relieved by NTG or rest
-some may be silent MIs
123
big 3 diagnostic tools for MI:
1. signs and symptoms
2. electrocardiographic changes
3. serum biomarkers
124
electrocardiographic changes in diagnosing MI
-ST elevation indicated ongoing hypoxia, cellular injury, ischemia (STEMI)
-no ST elevation, may have depressed ST or T wave changes (NSTEMI) better outcomes
125
serum biomarkers in diagnosing MI
-marker of choice to detect MI: elevated cardiac troponin 1 (cTnI)!
-elevated CPK-MB
126
myocardial infarction treatment
-reestablish blood flow and minimize damage
-reduce O2 demand and increase O2 supply
-MONA
-cardiac rehab
127
list 4 myocardial infarction complications
-dysrhythmias
-HF
-cardiogenic shock
-death, most occur before individual reaches hospital
128
acute coronary syndrome workup for STEMI
-ST elevation
-abnormal labs with biomarkers
129
acute coronary syndrome workup for NSTEMI
-no St elevation
-abnormal labs with biomarkers
130
acute coronary syndrome workup for unstable angina
-no ST elevation
-normal labs with biomarkers
131
what is endocardium
layer of endothelial cells that lines chambers of heart
132
infective endocarditis etiology
infection of endocardial structures by microorganisms which causes inflammation
-vegetations: large, bulky bacteria deposits on heart valves interfering function!
133
infective endocarditis clinical presentation
-non specific: low grade fever
-specific: petechiae!, splinter hemorrhages!, oslers nodes!, janeway lesions!, roth spots! (pictures on slide 99)
134
infective endocarditis diagnosis
-positive blood cultures
-echocardiogram
-murmur
-predisposing condition
135
infective endocarditis treatment
-6 weeks or more IV antibiotics
-surgery
-prophylactic antibiotics to prevent recurrence
136
myocarditis etiology
-inflammation and necrosis of cardiac muscle cells
-viral infections most common cause
137
myocarditis pathophysiology
-immune attack of the myocardium esp. the left ventricular wall
-muscles become flabby with necrotic tissue
-dilation of all 4 heart chambers
138
dilated cardiomyopathy
-enlargement of one or both ventricular chambers
-reduces contractility/EF
139
hypertrophic cardiomyopathy
-affects LV and septum
-exercise may cause obstruction of ventricular outflow and decreased CO
-risk of sudden cardiac death
140
restrictive cardiomyopathy
-stiff, fibrotic LV that resists filling
-decreased CO
-left side heart failure
141
pericarditis etiology
inflammation of pericardium resulting in fluid accumulation in pericardial sac
-thought to be viral cause
142
pericarditis clinical presentation
-systemic inflammatory response: fever, leukocytosis, tachycardia
-pericardial effusion
-friction rub: sticking/rubbing pain radiating back and forth like sandpaper!
143
compare normal pericardial space to cardiac tamponade in pericardial effusion
-normal pericardial space: 30-50mL
-cardiac tamponade: death 200mL or greater
144
Pericarditis treatment
-antibiotics
-aspirin
-NSAIDS
-steroids
145
Beck's triad with cardiac tamponade
from shock, need to get fluid off
-hypotension
-distended neck veins
-muffled heart sounds
-pulsus paradoxus: BP changes with RR
146
compare veins to arteries
carry blood to the heart
-have valves
-3 layers same as arteries
147
deep vein thrombus (DVT) etiology
virchows triad: venous stasis, vascular damage, hypercoagulability
148
deep vein thrombus (DVT) pathophysiology
-thrombus
-inflammation
-thrombus moves to lungs and causes pulmonary embolism
149
deep vein thrombus (DVT) clinical presentation
-condition causing problem
-redness
-ropiness
-tenderness
-warmth over vein
-Homans sign
150
deep vein thrombus (DVT) diagnosis
-clinical exam
-d dimer test: blood draw shows if clots are being broken down
151
deep vein thrombus (DVT) treatment
-prevention :antiembolism stockings, elevate, ambulation
-heparin, warfarin, factor Xa inhibitors
-greenfield filter
152
what are 5 indications of an arterial thrombus
-intermittent claudication
-cool to touch
-cyanotic
-arterial ulcer
-weak pulses
153
venous thrombus
-calf or groin tenderness
-swelling
-increased skin temp
154
chronic venous insufficiency etiology
valvular incompetence allowing back flow involving deep veins
-trauma, central obesity, pregnancy, prolonged standing
-pooling and stasis
155
chronic venous insufficiency clinical presentation
-venous stasis ulcers when superficial veins rupture: wet, irregular border!
-thin shiny skin
-dusky discoloration
-stasis dermatitis: blood cells leak out and cause discoloration!
-reduced or absent hair
156
chronic venous insufficiency diagnosis
doppler ultrasound, venography
157
chronic venous insufficiency treatment
-graduated compression!
-pneumatic compression
-anticoagulants
-thrombolytic agents
-venoablation
158
venous stasis ulcer from chronic venous insufficiency
from sluggish circulation and poor tissue oxygenation
-dark red, uneven margin, drainage
-treatment: exercise, compression stockings, topical medications
159
varicose veins etiology
high pressure
-prolonged standing
-sitting
-more women
-smoking
160
varicose veins pathophysiology
-valvular incompetence
-pressure on valves over time
-gravitational pull
-dont prevent backflow like they should
161
varicose veins clinical presentation
-aching, heavy discomfort
-bulging veins
162
varicose veins treatment
-elastic stockings
-elevate
-dont cross legs
-exercise
-sclerotherapy, vein stripping, vein ligation
163
