Basic Cardiac PPT Flashcards

1
Q

What is the number one cause of disease/death in the United States?

A

Heart disease

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2
Q

what is the primary role of the circulatory system?

A

maintaining blood flow and supplying oxygen to the body

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3
Q

what does the circulatory system delivery to all body cells?

A

oxygen, nutrients and other needed substances

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4
Q

what does the circulatory system remove from circulation?

A

removes the waste of metabolism

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5
Q

variations in ____ ____ and ____ __ ______ need to match the amount of blood flow in order to meet the changing demands of the body

A

heart rate;
force of contraction

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6
Q

when you are exercising, you are going to need more oxygen, thus there will be increased what?

A

blood flow

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7
Q

what happens to the pace of the circulatory system when we are sleeping?

A

it slows down

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8
Q

when there is any type of CVD, _____ ____ is going to be impaired and people will have issues

A

blood flow

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9
Q

what happens to the physical anatomy of the heart in pts with heart disease?

A

the heart enlarges and undergoes hypertrophy

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10
Q

the heart is basically the size of a ___ and weights how many pounds?

A

size of a fist and weights about a pound

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11
Q

the endothelium is the interface between what?

A

blood and artery wall

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12
Q

Endothelial cells have metabolic functions, list them:

(hint: 5)

A

Maintain vessel tone​

Hemostasis​

Angiogenesis​

Neutrophil chemotaxis​

Hormone secretion

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13
Q

what is angiogenesis?

A

the development of new blood vessels

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14
Q

neutrophil chemotaxis plays a role in our ______

A

immunity

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15
Q

what does the endothelium produce?

A

nitric oxide and endothelin

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16
Q

injury to the endothelium causes ___________

A

dysfunction

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17
Q

what is the thin layer of cells that lines the inner surface of all blood vessels?

A

endothelium

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18
Q

why do endothelial cells and blood vessels love nitric oxide?

A

it keeps endothelial tissue nice and smooth

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19
Q

List the functions of the epicardium/pericardium

(hint: 2)

A

keeps heart in place​

helps protect heart from trauma or infection

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20
Q

what are the characteristics of the epicardium/pericardium we discussed in class?

A

thin transparent outer layer of fibrous tissue​

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21
Q

in the epicardium/pericardium, receptors elicit reflex changes in what two things?

A

BP and HR

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22
Q

what layer of the heart is the thickest?

A

myocardium

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23
Q

what is the myocardium responsible for?

A

the actual pumping of the heart

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24
Q

what is the endocardium? what is it made up of?

A

inner layer that lines vessels of heart and made up epithelial tissue

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25
what valves are located between the atrial and ventricular chambers on each side?
atrioventricular valves
26
what do the atrioventricular valves prevent?
backflow into the atria when the ventricles contract
27
the mitral valve is also known as what?
bicuspid valve
28
what is the name of the left atrioventricular valve?
mitral (bicuspid) valve
29
the mitral valve consists of two ___, or ____, of the endocardium
flaps, or cusps
30
what is the name of the right atrioventricular valve?
tricuspid valve
31
the tricuspid valve consists of ____ flaps
three
32
what are the two semilunar valves?
pulmonic valve and aortic valve
33
what is the function of the semilunar valves?
they guard the bases of the two large arteries leaving the ventricular chambes
34
each cardiac cycle consists of 3 sequential events that occur within how long? what are these events?
within less than a second, usually 0.8 seconds 1. diastole 2. atrial systole 3. ventricular systole
35
the cardiac cycle = ?
one complete heartbeat
36
list the steps of the cardiac cycle (hint: 6)
1. atrial systole begins 2. atrial systole ends and atrial diastole begins 3. first phase of ventricular systole 4. second phase of ventricular systole 5. early ventricular diastole 6. late ventricular diastole
37
what happens in atrial systole?
atrial contraction forces a small amount of additional blood into relaxed ventricles
38
what happens when atrial systole ends and atrial diastole begins?
the atria relax
39
what happens in the first phase of ventricular systole?
ventricular contraction pushes AV valves closed but does not create enough pressure to open semilunar valves
40
what happens in the second phase of ventricular systole?
as ventricular pressure rises and exceeds pressure in the arteries, the semilunar valves open and blood is ejected
41
what happens in early ventricular diastole?
as ventricles relax, pressure in ventricles drops; blood flows back against cusps of semilunar valves and forces them closed. blood flows into relaxed atria
42
what happens in late ventricular diastole?
all chambers are relaxed; ventricles fill passively
43
during diastole, both the atria and ventricles relax, allowing what?
blood to flow into heart
44
diastole is about ___ of cardiac cycle
2/3
45
during systole, the heart contracts and does what?
pumps blood out of heart
46
what is cardiac output?
the amount of blood the heart pumps (ejects) per minute from the left ventricle
47
what is stroke volume?
the amount of blood pumped by the ventricles with each heartbeat
48
average heart rate = ?
60 to 130 per minute
49
what two things play a role in heart rate?
nerves and hormones
50
what is the normal amount of cardiac output per minute?
4-8 L
51
cardiac output is measured by ____ ____ & _____ _____
heart rate & stroke volume
52
Can stroke volume be directly measured?
No
53
What 3 factors impact stroke volume, thus impacting cardiac output?
preload, afterload and contractility
54
stroke volume is influenced by ____ volume and _______ ________
blood; vascular resistance
55
what is preload also known as?
left ventricular end diastolic pressure
56
preload is the _______ of muscle fibers in the _______ to the greatest of their ability
stretching; ventricles
57
what does the stretching in preload depend on?
the amount of blood in the ventricle at the end of diastole, or when the mitral valve closes
58
what is frank starling's law?
The more the heart muscles stretches during diastole the more forcefully it will contract at systole.​
58
During preload, the more _____ the greater the _______
blood; stretch
59
under frank starling's law, the stretch increases to accommodate what?
greater volume
60
under frank starling's law, the stretch increases _______ ______, increases the __________ of ______ ions, and creates a _______ _______
sarcomere length; sensitivity of calcium ions; strong contraction
61
Does frank starling's law refer to preload or afterload?
preload
62
the more the heart fills, the more ________. therefore, a stronger ________, and a larger _____ _______
preload; contraction; stroke volume
63
What factors affect preload, or increased ventricular filling? (think of the chart on slide; hint: 6)
increased ventricular compliance increased atrial contractility increased aortic pressure increased central venous pressure decreased heart rate decreased ventricular inotropy
64
what two factors influence increased central venous pressure?
decreased venous compliance increased thoracic venous blood volume
65
what factors increase preload? (hint: 8)
Increased central venous pressure​ Reduced heart rate​ Valvular regurgitation ​ Increased aortic pressure​ Ventricular systolic heart failure​ Increased circulating volume​ Mitral insufficiency​ Aortic insufficiency
66
What factors decrease preload? (hint: 7)
Decreased central venous pressure​ Increased heart rate​ Decreased circulating volume​ Mitral stenosis​ Vasodilator use (Nitro)​ Atrial fib​ Cardiac tamponade​
67
what is contractility?
Ability of the myocardium to contract normally (squeezing of the ventricles)​
68
What causes decreased circulating volume? (hint: 2)
Bleeding Third Spacing
69
increased contractility causes an increase in what?
stroke volume
70
contractility is influenced by _______
preload
71
positive inotropy = ?
increased force of contraction
72
negative inotropy = ?
decreased force of contraction
73
the bigger the preload the better the ________
contraction
74
when you hear the term inotropy, think _______
contraction
75
what is afterload?
the amount of resistance the heart must pump against when ejecting blood
76
to eject blood out of the left ventricle, the aortic valve has to open to push it to the body. there is vascular resistance. this represents _______
afterload
77
In heart failure, your heart is not _________ great so it has to work much harder to open up the aortic valve
contracting
78
What happens when afterload is low?
the workload is easier; the ventricle does not have to exert much effort to get the blood out of the heart
79
what BP reading would represent low afterload?
normal BP 110/60
80
What happens when afterload is high?
vasoconstriction occurs; afterload is increased due to increased systemic vascular resistance
81
what BP reading would represent high afterload?
hypertension (BP 180/90)​
82
When the heart starts to fail, there is more blood going into the heart than leaving it. What can this lead to?
cardiomyopathy, hypertrophy, enlarged heart
83
what does remodeling mean in the heart?
chronic pathologic changes to the structure and function of myocardium or heart tissue
84
what heart issues can cause remodeling that we discussed in class?
hypertension, heart failure, heart attacks
85
When people have heart disease and the heart has to do extra work, what physical change occurs?
the heart will get larger (hypertrophy)
86
what is the normal ejection fraction range?
55 to 70%
87
what ejection fraction number is abnormal?
anything below 40%
88
ejection fraction = ?/?
amount of blood pumped out of ventricle (SV) / total amount of blood in the ventricle (preload)
89
if someone has an abnormal ejection fraction, what is occurring?
their heart is not putting out a lot of oxygenated blood to the rest of the body
90
why does the SNS secrete epinephrine and norepinephrine?
to increase blood flow to the heart, lungs, brain, and skeletal muscles​
91
In stressful situations, the SNS is activated to get more ______ to the tissue
oxygen
92
in stressful situations, the SNS will be activated to do what?
speed up heart rate increase BP
93
Beta 1 receptors impact what 3 parts of body?
kidneys, heart, and adipose tissue
94
how do beta 1 receptors impact kidneys?
renin release
95
what do beta 1 receptors influence on the heart?
rate force automaticity cardiac output
96
how do beta 1 receptors impact adipose tissue?
lipolysis
97
when the beta 1 receptor is activated, there is increase in the ____ and ____ of myocardial contraction. Excess stimulation leads to _________
force and rate; arrhythmias
98
beta receptors are primarily responsible for signaling what?
sympathetic nervous system
99
when beta 1 receptors are stimulated, HR and contractility are increased. This is then going to increase _____ ______ and _____ ______
stroke volume; cardiac output
100
what effect does beta blocker medications have on HR and force of contraction?
they decrease HR and force of contraction
101
beta 2 receptors impact what 3 parts of the body?
Smooth muscle, blood vessels, and liver
102
how do beta 2 receptors impact smooth muscle?
causes relaxation
103
how do beta 2 receptors impact blood vessels?
causes vasodilation
104
how do beta 2 receptors impact the liver?
causes glycogenolysis
105
when beta 2 receptors are activated, how do they impact the airway?
they cause broncodilation and a decrease in airway resistance
106
when beta 2 receptors are activated they cause relaxation of what types of smooth muscle?
both vascular and non-vascular smooth muscle
107
beta 2 receptors play a role in _______ metabolism
glucose
108
RAAS is a hormone signaling system that regulates _____ ______
blood volume
109
dehydration, sodium deficiency or hemorrhage causes a decrease in what?
blood volume
110
if there is a decrease in blood volume there is also a decrease in what?
blood pressure
111
when dehydration, sodium deficiency or hemorrhage causes decreased blood volume and decreased blood pressure, there will then be increased ______
renin
112
what are the 3 main substances of RAAS?
renin (enzyme), aldosterone (hormone), and angiotensin II (hormone)​
113
when the body senses something, like dehydration, sodium deficiency, or hemorrhage, what organ notices first?
kidneys
114
the 3 main substances of the RAAS help regulate BP how?
by increasing sodium reabsorption, water reabsorption, and vascular tone
115
when we talk about vascular tone, this means how much do the blood vessels _____
constrict
116
how much cardiac output do the kidneys account for?
20%
117
when BP is low, the kidneys will sense that and release ____ into the bloodstream
renin
118
when renin is released, it is going to split into _________ and go to the _____
angiotensinogen; liver
119
angiotensinogen will cause an increase in __________
angiotensin I
120
What form of angiotensin is inactive?
angiotensin I
121
angiotensin I splits off and goes to the _____ and releases what?
lungs; angiotensin converting enzyme (ACE)
122
What form of angiotensin is active?
angiotensin II
123
When angiotensin II becomes active, what does it cause?
vasoconstriction which then increases blood pressure
124
When angiotensin II becomes active, it triggers the release of substances by different glands. Explain this and what it causes.
It triggers adrenal gland to release aldosterone and the pituitary gland to release ADH which then in turn causes the kidneys to retain sodium which leads to water retention, this causes BP to increase and increase in blood volume bc holding on to extra water ​
125
Aldosterone and angiotensin II play a role in stimulating what?
SNS
126
The RAAS is constantly activated in people with chronic inflammation. What can this lead to?
the shredding of blood vessels and the development of atherosclerosis
127
what is a major vasoconstrictor and shredder of blood vessels?
angiotensin II
128
ACE inhibitors prevent the secretion of ________
angiotensin II
129
inappropriate RAAS activation can cause impaired _________ and ________ health
vascular and metabolic
130
increased angiotensin II causes ________ dysfunction and ________ remodeling. It also causes impaired ___________
endothelial; vascular; adipogenesis
131
Increased angiotensin II can lead to impaired adipogenesis which then causes what?
glucose intolerance
132
increased angiotensin II can lead to endothelial dysfunction and vascular remodeling which can lead to what?
elevated BP and atherosclerosis
133
Inappropriate RAAS activation can lead to shredding of ____ ______, the development of __________ _______, and _______
blood vessels; atherosclerotic plaque; hypertension
134
fat cells (adipose cells) have a lot of pro-inflammatory mediators which leads to chronic inflammation. what can this lead to?
diabetes, other heart diseases, insulin resistance, etc
135
aldosterone causes increased water and sodium retention which leads to increased _______
preload
136
angiotensin II causes constriction of vascular smooth muscle which leads to increased _______
afterload
137
what are the 5 characteristics of metabolic syndrome?
Hypertension​ ​ Obesity​ ​ Abnormal cholesterol levels​ ​ Chronic inflammation​ ​ Insulin resistance
138
usually you can look at someone and tell if they are at risk for metabolic syndrome. what things did we discuss in class regarding this? (hint 3 things)
usually someone over 50 usually overweight may have comorbidites
139
when looking at someone who is overweight, where they carry weight on their body can increase risk of metabolic syndrome. where would this weight be?
chest abdomen area with more visceral fat in abdominal area
140
insulin resistance is when cells do what?
fail to make effective use of insulin
141
In someone with insulin resistance, blood sugar _______
increases
142
in someone with insulin resistance, what cells secrete insulin?
beta cells in the pancreas
143
what is the expected outcome in someone who does not have insulin resistance?
the glucose will reduce with insulin secretion and insulin levels decrease.​
144
in someone with insulin resistance, insulin is not able to reduce _____ ______. The compensatory insulin fails as well and the person remains __________.​
blood sugar; hyperglycemic
145
without insulin, you cannot make _____ ______ which is needed to keep endothelial cells nice and smooth
nitric oxide
146
Without insulin, you cannot get glucose to where it should be. We want glucose in ____ and not in ________
cells; circulation
147
What does insulin resistance cause? (hint: 5)
Increase catecholamine​ Stimulates sodium reabsorption​ Endothelial dysfunction​ RAAS and SNS dysfunction​ Increase in smooth muscle proliferation
148
insulin resistance can stimulate sodium reabsorption. what effect can this have on BP?
increases BP
149
Insulin resistance increases smooth muscle proliferation. what can this lead to?
hypertrophy and target organ damage
150
blood pressure often decreases with meds that improve _______ ________
insulin sensitivity
151
what medications often improve insulin sensitivity?
ACE inhibitors
152
Why is insulin helpful in vascular protection?
it promotes increased endothelial cell production of nitric oxide
153
List the genetic and environmental factors on the "cycle of death" (hint: 7)
insulin resistance RAAS Sodium Stress SNS Inflammation Obesity
154
what can the cycle of death lead to? (hint: 2)
vasoconstriction increased renal sodium & water retention (triggering of RAAS)
155
The cycle of death can lead to vasoconstriction. What does this cause?
increased peripheral and systemic vascular resistance
156
The cycle of death can lead to increased renal sodium & water retention. What does this cause?
increased fluid/blood volume
157
How does the cycle of death affect preload and afterload?
Vasoconstriction causes increased afterload Increased renal sodium & water retention causes increased preload
158
obesity & adipose tissue leads to a low-grade chronic inflammatory state. what can this cause? (hint: 4)
CVD (increased thrombosis) Type 2 Diabetes Hypertension Hyperlipidemia
159
what causes obesity to lead to chronic inflammation?
the mediators that the adipose tissue hold that trigger your immune system to be constantly revved up more than it should be.
160
What can target organ damage cause? (hint: 6)
Left Ventricular Hypertrophy Atherosclerotic Cardiovascular Disease Peripheral Artery Disease Retinopathy Renal issues Brain issues
161
how can an eye doctor tell if you have hypertension?
they look at the back of the retina. the blood vessels on your retina should be nice and smooth, but if they are really jagged or if they are enlarged that is indicative of hypertension​
162
Target organ damage is believed to increase the risk of what? why does this make sense?
dementia if there is decreased circulation then there is decreased O2 getting to tissues which can also decreased in brain​
163
List the risk factors for CVD (hint: 9)
Hypertension Genetic susceptibility Obesity Smoking Age Stress and tension Diabetes Physical inactivity Hyperlipidemia
164
Endothelial injury causes _______
dysfunction
165
what does an endothelial injury start/trigger?
inflammatory response
166
when an endothelial injury occurs, what is inhibited?
the release of nitric oxide
167
Endothelial injury causes increased levels of what?
Von Willebrand Factor (vWF)
168
Von Willebrand Factor (vWF) is a marker of what?
endothelial damage/dysfunction
169
Endothelial dysfunction is anything that will ______ _____ ______
shred blood vessels
170
what is atherogenesis?
the development of atherosclerotic disease
171
Risk factors for CVD can cause ________ _______ which then causes _________
endothelial dysfunction; atherogenesis
172
Step 1 Endothelial Injury: an endothelial injury causes what to come to the site?
platelets, macrophage and inflammatory mediators
173
Step 2 Endothelial Injury: what is deposited on the injured area when there is an endothelial injury?
LDLs
174
Step 3 Endothelial Injury: what develops at the injury site?
FOAM cells
175
FOAM cells = ? + ?
oxidized LDL + macrophages
176
Explain how FOAM cells are formed
when macrophages engulf excessive lipids, primarily LDLs
177
Step 4 Endothelial Injury: ________ _____ forms and _______ occurs to the smooth muscle wall of artery
aterosclerotic plaque; hypertrophy
178
Step 5 Endothelial Injury: What decreases?
vasodilation capacity
179
Step 6 Endothelial Injury: plaque ______ with time, ______ easily, and pieces of plaque _____ _____ and travel
calcifies; fissures; break off
180
how does an embolism occur?
pieces of plaque breaks off artery wall and travels
181
____ ____ lay the foundation for atherosclerotic disease
FOAM cells
182
When plaque continues to build up, this will lead to _________ because the blood still needs to get through and the vessels can only stretch so far
hypertrophy
183
what does a total blockage of a blood vessel lead to?
heart attack
184
In CAD, LDL deposits ________ between layers in the artery wall
cholesterol
185
when cholesterol is deposited into artery wall, what occurs?
inflammatory cells (macrophages) engulf deposited cholesterol and then become giant FOAM cells
186
If plaque ruptures where can it travel that is dangerous? what things can occur?
other parts of heart, lungs, brain pulmonary embolism, stroke, heart attack
187
at the site of a plaque rupture, what forms?
a blood clot (thrombus)
188
when there is a plaque rupture, what happens to the myocardium?
the heart muscle supplied by the blocked artery starts to die
189
What causes symptoms of a coronary blockage?
they all come from inadequate tissue perfusion; disruption of supply and demand
190
When there is a coronary obstruction, there is a blockage or obstruction of a main organ. What can this cause? (hint: coronary, peripheral disease, cerebral)
Coronary​ - Stable Angina​ - Unstable Angina​ ​ Peripheral Disease​ - Claudication​ ​ Cerebral​ - Transient Ischemic Attack - Cerebrovascular Accident, or Stroke
191
What is the bottom line when knowing the difference between stable vs unstable angina?
stability of the plaque
192
List characteristics of unstable angina (hint: 4)
usually a new onset of angina chest pain at rest (never had it before) angina with less exercise or less exertion than before chest pain usually not relieved with nitroglycerin ​
193
unstable angina is considered a precursor or warning sign to what?
that you are having a myocardial infarction soon
194
what type of angina would have a significant fixed lesion?
stable angina
195
List re-perfusion strategies (hint: 6)
Pharmacologic agents (fibrinolytic therapy)​ ​ Percutaneous transluminal coronary angioplasty (PTCA)​ Stent​ Atherectomy​ Thrombectomy​ ​ Coronary Artery Bypass Graft (CABG)​
196
what is fibrinolytic therapy and how long do you have to do this?
fibrinolytic drug is given to totally break up the clot. But you only have 60 mins from the onset to get this done. ​
197
What is the 5th most common procedure in the US for re-perfusion?
Percutaneous coronary intervention
198
what happens during percutaneous coronary intervention?
Think of it has a cardiac catherization. They go in either in your femoral artery or nowadays radial artery, and thread a catheter into your heart with a balloon.
199
what is percutaneous coronary intervention also called sometimes?
balloon angioplasty
200
Explain how a stent is placed and how it works
They will thread the catheter in while the balloon is deflated. Then they will have a very small stent and expand the balloon what it will do is push the plaque out of the way, reopening the blood vessel and they will put the stent in place. The stent will expand and then they deflate the balloon and remove the catheter. They leave the stent in place.
201
A patient with hypovolemic shock is given IV fluids. IV fluids will help _________ cardiac output by _______ preload
increase cardiac output by increasing preload
202
Which category of beta blockers inhibit both beta 1 and beta 2 receptors? What category of beta blockers inhibit primarily beta 1?
non-selective beta blockers inhibit both beta 1 and beta 2 selective beta blockers inhibit primarily beta 1