Module 7 Flashcards
1
Q
Lymphatic System carries things …
A
too large to cross the capillary membrane
2
Q
Right Lymphatic Duct
A
Top right quarter of the body drains here
3
Q
Thoracic Duct
A
where 3/4 of lymph drains into
4
Q
What is the “pump” and “pipes/tubes” of the cardiovascular system?
A
Blood vessels are the pipes and the heart is the pump
5
Q
What is the function of the circulatory system
A
To deliver O2, nutrients, and other substances to all body cells
Remove waste products of cellular metabolism
6
Q
Intrinsic Regulators of the Circulatory System
A
Nervous System
Endocrine System
7
Q
How does the circulatory system interact with the digestive system?
A
Digestive system supplies the nutrients
8
Q
How does the circulatory system interact with the respiratory system?
A
Supply O2, Remove CO2, Maintain acid-base balance
9
Q
How does the circulatory system interact with the renal system?
A
Waste removal from blood, fluid and electrolyte balance, and acid base balance
10
Q
Pulmonary Circulation
A
Right heart pumping deoxygenated blood to the lungs for gas exchange
11
Q
Systemic Circulation
A
Left heart pumping oxygenated blood to the rest of the body for delivery of O2 and nutrients and removal of wastes and CO2
12
Q
Arteries
A
Carry blood AWAY from the heart
13
Q
Capillaries
A
closest contact and level of EXCHANGE between the blood and interstitial space (interstitium) or the cellular environment
14
Q
Veins
A
Carry blood TOWARD the heart
15
Q
Lymphatics
A
carry plasma from the interstitium to the heart
16
Q
How are vessels named (arteries, veins, etc)?
A
After their direction of flow, not whether they carry oxygenated/deoxygenated blood (since the pulmonary artery carries deoxygenated and pulmonary veins pump oxygenated blood)
17
Q
Arteriovenous Malformation
A
condition where arteries and veins attach / get tangled up and disrupt normal blood flow (normal exchange thus cannot occur without that capillary there)
18
Q
Where does the heart lie?
A
obliquely (at an angle) in the mediastinum (area above diaphragm and between the lungs; forces left lung to be different from right)
19
Q
Dextrocardia
A
when someone’s heart is on the RIGHT instead of the left
20
Q
Size and Weight of the heart?
A
Less than a pound and about the size of a fist
21
Q
Functions of the Heart Wall and Fibrous Skeleton?
A
Enclose and support heart (allow heart to stay in place)
Divide the heart into 4 chambers
Possesses the valves and great vessels
22
Q
Function of Valves
A
direct blood flow through opening and closing (issues may lead to backflow)
23
Q
Function of great vessels
A
conduct blood to and from the heart cells
24
Q
Coronary Circulation
A
Part of systemic circulation
Arteries and veins that serve the metabolic needs of the heart cells through coronary vessels that branch and penetrate the heart
25
What blood is NOT a part of coronary circulation?
Any blood pumped elsewhere in the body
Blood in the ventricles and inside the heart do not supply coronary circulation
26
Nodes
specialized heart cells that generate action potentials (sinoatrial and atrioventricular)
27
Function of Nerves and Specialized Muscle Cells in the Heart?
direct rhythmic contraction and relaxation and propel blood through pulmonary and systemic circuits
28
Ectopic Beat
a beat that lies outside the specialized heart cells and does not follow the normal electrical pathway
Basically, an extra beat before a normal beat (common and may feel like an extra beat or like your heart is skipping a beat)
29
Intercalated Discs
microscopic discs connecting cells of the heart to allow impulses to travel through the cells for rapid depolarization, and allow muscles to contract simultaneously in the right and left side in order to give a coordinated pump
30
Pericardium
Double walled membranous sac that encloses the heart (we have parietal and visceral)
(similar to the pleural lining in the lungs if you think about it)
31
Parietal Pericardium
OUTER layer of the sac surrounding the heart
It is a surface layer of mesothelium over a thin layer of connective tissue
32
Visceral Pericardium
INNER layer of the sac surrounding the heart
Folds back AND is continuous with the parietal pericardium to allow large vessels to enter/exit the heart without breaching the layers / not let any fluid leak out
33
Pericardial Cavity
Fluid containing space between visceral and parietal pericardium
34
Pericardial Fluid
secreted by the cells of the mesothelium to lubricate membranes and minimize friction as the heart beats
35
Epicardium
another name for the visceral pericardium - outermost heart layer
36
Pericardial Effusion
Fluid entering the pericardial membrane and building up - thus preventing effective heart beating
37
Functions of the Pericardium
1. Prevents displacement of the heart during gravitational acceleration/deceleration
2. Provides physical barrier against infection and inflammation from the lungs and pleural space
3. Contains pain and mechanoreceptors that elicit reflex changes in BP and HR
38
Mechanoreceptors (in the heart)
stretch receptors in the atria (muscles) that can respond to overstretching (ex: with too much blood coming back in)
As a response they secrete atrionaturitic factor which directs the kidneys to get rid of sodium (which water follows) to decrease volume and ease the heart
39
Pain Receptors (in the heart)
React to low oxygenation in the heart - when the heart muscle is starved - which leads to anginal pain
40
Myocardium
Actual Cardiac Muscle
Anchored to the heart's fibrous skeleton
Thickness varies between chambers, and is r/t the amount of resistance that area of muscle must overcome to pump blood from the different chambers
41
Thickest myocardial wall?
Left Ventricle - it has to go against systemic blood pressure (120/80)
42
Why is the right ventricle wall not as thick as the left?
It is about as thick as the right atrial wall because it only needs to push against pulmonary pressure (25/10) which is a great difference from the systemic pressure of the left
43
Endocardium
Internal lining composed of connective tissue and squamous cells
It is smooth so that way the blood flow is smooth through the heart (its the layer touching the blood inside)
44
What kind of circuit does the endocardium make ?
a continuous closed circuit
it is continuous with the endothelium that lines arteries, capillaries, and veins
45
What can a lack of a closed circuit lead to ?
Debris collection and clotting (atherosclerosis)
46
How do the atria differ from the ventricles?
they are smaller with thinner walls (R - 2 mm , L - 3-5 mm)
47
Atria
thinner walls of the heart
serve as storage units and conduits (passive filling) for blood
offer little resistance to flow of blood into ventricles
48
What sort of processes occur in the atria ?
Passive Processes - but, there is a tiny atrial contraction (kick) at the end
49
What can atrial failure lead to ?
Decrease in cardiac output
50
Ventricles
Thicker myocardial layer making up the bulk of the heart (R- 3-5 mm; L- 13-15 mm)
Propel blood through pulmonary and systemic circulation
Right and left are shaped differently
51
Mean Pulmonary Pressure
about 15 mmHg
52
Mean Arterial Pressure
about 92 mmHg
53
What is the most muscular portion of the heart?
Left Ventricle
54
What can ventricular failure lead to?
DRASTIC decrease in cardiac output
55
Right Ventricle shape
shaped like a crescent or triangle and acts like a bellows to propel large volumes of blood through a very small valve into the low pressure pulmonary circulation
56
Left Ventricle shape
Larger and Bullet shaped
pumps blood through a large valve opening into the higher pressure systemic circulation
57
Septum
separates the sides of the heart
also carries the bundle of HIS beyond the AV node
58
Interatrial Septum
Separates the right and left atrium
59
Interventricular Septum
Separates the right and left ventricles
It is an extension of the fibrous skeleton of the heart
60
What are heart valves?
Indentations of the endocardium
Separate the atria from the ventricles (AV) and the ventricles from the aortic and pulmonic arteries (Semilunar)
61
When do heart valves open and close?
With pressure changes within the chambers
62
Atrioventricular valves
AV Valves
open at the beginning of Diastole and allow blood to fill the ventricles
Close at the beginning of ventricular contraction to prevent backflow of blood into the atria
63
Semilunar Valves
open at the end of ventricular contraction when the pressure in the ventricles exceed the pressure in the pulmonary artery and aorta
Close at the beginning of ventricular relaxation as the pressure in the chambers drops below the pressure in the pulmonary artery and aorta to prevent backflow of blood into the ventricles
64
AV Valves open at the start of ___
Diastole (which is the ventricular filling)
65
AV Valves close at the beginning of ___ ___
ventricular contraction
66
Semilunar valves open at the end of ___ ___
ventricular contraction
67
Semilunar valves close at the beginning of ___ ___
ventricular relaxation
68
Chordae Tendinae
connect valve leaflets or cusps to papillary muscles (extension of the myocardium)
69
Papillary Muscles
Extensions of the myocardium that pull the cusps or leaflets together and downward at the beginning of ventricular contraction to prevent backward expulsion of the AV valves into the atria
They hold the leaflets closed during ventricular contraction
70
The ventricles are NEVER what ?
Fully emptied of blood
71
When the atrial kick occurs, pressure in the ventricles ___ and they will contract as the ____ valves close. ___ valves then open to do contraction firing of blood from the ventricles, making the pressure ____
rises ; AV ; Semilunar ; Drops
72
What are the two AV valves
Tricuspid and Mitral
73
What are the two semilunar valves
Pulmonic and Aortic
74
Largest diameter valve
Tricuspid
75
Valve resembling a cone shaped funnel
Mitral
76
Valves behave like..
one way swinging doors
77
Valves with 3 cup-shaped cusps
Pulmonic and Aortic
78
Pulmonic cusps are ___ than aortic
thinner
79
Great Vessels include ...
Superior and Inferior Vena Cavae
Pulmonary Artery
Pulmonary Vein
Aorta
All are part of systemic circulation, but in reality pulmonary artery and vein are not since they handle blood from an to the lungs
80
Superior and Inferior Vena Cavae
Enter the right atrium
81
Pulmonary Artery
carries deoxygenated blood from the right ventricle to the lungs
82
Pulmonary Vein
carries oxygenated blood from the lungs to the left atrium
83
Aorta
delivers blood to systemic vessels which carry it to the rest of the body
84
Diastole
Relaxation Phase
Blood fills the ventricles as it passively flows through the atria
85
Systole
Contraction phase
Blood pumped out of the ventricles into circulations
86
Why is there a split in ventricle ejection between left and right?
Right ejection occurs slightly earlier due to pressure differences and the size of the lumen being different
87
What occurs first, atrial systole or ventricular systole?
Atrial Systole
88
What leads to atrial contraction/atrial kick?
Blood enters the atria from vena cavae and coronary sinuses to the right side --> on the left blood enters through 4 pulmonary veins (2 L and 2R) --> The atria fill up and distend --> AV valves open --> Blood passively fills the ventricles --> Atrial kick actively then pumps additional blood into the ventricle before ventricular contraction occurs
89
If there is no atrial kick, what can happen?
You can lose 25 mL
90
Most ventricular filling occurs during ...
the first third of ventricular diastole (its a passive fill)
91
Phases of the Cardiac Cycle
4 Phases
92
Phase 1 of the Cardiac Cycle
"Isovolumetric Contraction"
This starting point is ventricular systole
Ventricular volume is constant and the increase in pressure due to this closes the AV valves
93
Phase 2 of the Cardiac Cycle
The semilunar and AV valves are initially closes as the ventricles squeeze on blood to raise pressure, which causes the semilunar valves to open as the ventricles contract and eject blood into circulation
Intraventricular volume and pressure decrease
94
Phase 3 of the Cardiac Cycle
Isovolumetric Relaxation
Semilunar valves close as the pressure goes down and the ventricles relax (but not all blood leaves the heart)
Pressure decreases in the ventricles, semilunar valves close, ventricles relax
95
Phase 4 of the Cardiac Cycle
Decrease in ventricular pressure opens the AV valves
This leads to passive ventricular filling from the atria into the ventricles followed by the kick
96
Isovolumetric Ventricular Relaxation and Filling
Diastole (Phase 3)
0.4 Seconds
Once ventricles relax after systole, pressure drops below that in arteries making semilunar valves close
When pressure in ventricles drops below that in atria, AV valves open and allow for ventricular filling
Toward the end of diastole, the atria contract (kick) and eject 25% more blood volume into the ventricles (0.1 s)
97
Isovolumetric Ventricular Contraction and Ejection
Systole (0.3 s)
Pressure in ventricles became greater than atria, so the AV valves shut and isovolumetric contraction of the ventricles occurs
As pressure increases and becomes greater than the arteries, the semilunar valves open and blood is ejected into the pulmonary and systemic circulation
98
The First Heart Sound
0.14 seconds
This is the S1 and when the AV valves shut at the beginning of systole due to increasing pressure in the ventricles
The actual sound is because the valve shuts which makes surrounding tissue vibrate which makes blood flow turbulent in the area causing the LUB
99
The Second Heart Sound
0.10 seconds
This is the S2 and when the Semilunar valves shut at the end of systole due to falling pressure in the ventricles
100
Amount of blood circulated?
5 Liters
101
Physiologic Split
The aortic valve closes before the pulmonic valve during S2 by 0.02 to 0.04 to 0.06 sec during expiration and inspiration
This is to allow the same amount of volume to be pumped through both the pulmonary artery and aorta (the aorta lumen is larger) so basically the pulmonary artery gets more time pumping
102
What are the valves doing during Systole?
AV valves are closed (S1)
| SL valves are open
103
What are the valves doing in Diastole?
AV valves are open
| SL valves are closed (S2)
104
S1 is heard...
as first heart sounds when the AV valves close
105
S2 is heard...
as second heart sounds when SL valves close
106
S3
can be heard as a third heart sound ventricular wall compliance is decreased and structures in the ventricular wall vibrate
The wall is stiff leading to extra noise on filling the atria or tensing of tensae chordae
Is not necessarily a non-normal finding
107
When is S3 a normal finding?
If its found in individuals younger than 30 years of age - its like how a new baseball glove has less give than a used one - it is not necessarily pathonomic
108
What conditions COULD cause S3?
congestive heart failure
| valve regurgitation
109
S4
A fourth heart sound
NEVER NORMAL, ALWAYS BAD
can be heard on atrial systole if resistance to ventricular filling is present
may sound like DE LUB DUB (DE LUB DUB DUB if S3 is present)
110
What may cause S4?
Not so much related to heart failure
Related to:
Cardiac Hypertrophy
Disease
Injury or Ventricular Wall
111
Blood in the heart chambers ...
does NOT supply O2 or nutrients to heart cells
112
Coronary Ostia
openings in the aorta that direct blood into coronary arteries
113
Coronary Sinus
an opening into the right atrium from the coronary veins
114
Coronary Arteries
Traverse the epicardium and branch several times to provide the heart with O2 and nutrients
115
Parts of the Right Coronary Artery
Conus
Right Marginal Branch
Posterior Descending Branch
116
Parts of the Left Coronary Artery
LAD
| Circumflex Artery
117
Conus
right coronary artery
supplies blood to upper right ventricle
118
Right Marginal Branch
right coronary artery
traverses right ventricle to the heart apex
119
Posterior Descending Branch
right coronary artery
supplies smaller branches to both ventricles
120
LAD
Left Anterior Descending Artery (anterior interventricular artery)
Supplies blood to portions of the left and right ventricles and much of the interventricular septum
121
Widowmaker
An LAD blockage that can cause the ventricles to die and often kill a person
122
Circumflex Artery
Left Coronary Artery Branch
Supplies blood to the left atrium and lateral wall of the left ventricle
123
The right and left coronary arteries feed ...
not just the muscles (mechanical part) of the heart, but also the electrical parts
124
Collateral Arteries
connections between two branches of the same coronary artery or connections of branches of the right and left coronary arteries
Form as a part of angiogenesis
125
When do collateral arteries spawn?
As we age and grow they are made through angiogenesis
126
What happens if atherosclerosis plaque is blocking a coronary artery?
collateral arteries via angiogenesis forms to allow new mediums of blood movement
they flow around blockages to still allow blood to flow
127
What heart layer has more collateral arteries?
epicardium has more than endocardium
128
Collateral circulation ____ the heart
protects
129
What can help form collateral arteries after an MI?
monitored exercise
130
What is the difference in mortality between MI in young and older people?
Younger people with MI are more likely to die because they have not yet formed the collateral arteries like an older person has
131
At what level does coronary circulation exchange occur?
the coronary capillaries
132
How many capillaries are there ?
1 PER CARDIAC MUSCLE CELL
3300 Capillaries per square millimeter
133
Why is cardiomegaly/hypertrophy so dangerous?
The increase of the heart muscle's size is not accompanied by more coronary capillaries, so there is a supply and demand issue - the capillaries have to perfuse a larger area they were not designed to perfuse so O2 and nutrient exchange decreases thus causing hypoxia and angina
134
Coronary Veins
Most venous drainage occurs through these veins in the visceral pericardium
135
Great Cardiac Vein
smaller coronary veins feed into this greater vein which empties into the right atrium through the coronary sinus
136
Coronary Lymphatic Vessels
With cardiac contraction, lymphatic vessels drain fluid to lymph nodes in the anterior mediastinum which eventually will empty into the superior vena cava
This is important for protecting the myocardium against injury
137
Cardiac Conduction System Path
Electrical Impulse --> Fiber Shorten --> Muscle Contraction --> Systole
Post Action potential --> Fibers relax --> return to resting length --> Diastole
138
The heart contains specialized cells that generate ...
its own action potentials without stimulation from the NS
139
The heart has its own ___ system
conduction
140
Nodes
concentrated areas of specialized cells in the heart that generate AP
141
What provides regulation for the heart's conduction system?
ANS via SNS and PNS nerve fibers that effect heart rate and diameter of coronary vessels
142
____ & ____ affect strength and duration of Myocardial contraction and relaxation
Hormones and Biochemicals
143
The conduction system requires a lot of ...
O2 and nutrients since it is always beating the heart
144
Cardiac cells have what 3 things that are not true of muscle cells?
1. Automaticity
2. Excitability
3. Conductivity
145
Automaticity
can generate and discharge an electrical impulse
146
Excitability
can respond to an electrical impulse
147
Conductivity
ability to transmit an electrical impulse from one cell to the next cell
148
Chronotropic
Heart Rate
149
Inotropic
Heart Contraction (Strength)
150
Dromotropic
Heart Conduction (Speed)
151
What receptors in the heart interact with EP and NEP?
Beta 1 is the predominant kind
152
Another name for EP and NEP?
Adrenaline/Noreadrenaline
153
SNS effects on Chrono/Ino/Dromotropic
Increases all
154
PNS effects on Chrono/Ino/Dromotropic
Decreases all
155
What receptor and neurotransmitter is used in the PNS on the heart?
Muscarinic receptors and Acetylcholine (cholinergic receptors)
156
What receptor and neurotransmitter is used in the SNS on the heart?
Beta 1 receptors and EP/NEP (Adrenergic Receptors)
157
Pacemaker of the Heart
Sinoatrial Node (SA Node) - which has the highest activity for generating a signal through depolarization of cells
158
Where is the SA node found?
Almost where the vena cavae come into the heart
159
AP Pathway in the Heart?
SA Node --> AV Node --> Bundle of HIS --> Bundle Branches --> Purkinje Fibers
160
What bpm can the SA node generate?
70-75 bpm
161
What bpm can the AV node generate?
50 bpm (so if the SA node does not work there is a lower signal / chronotropism as a result)
162
What bpm can the purkinje fibers generate?
15-30 bpm (which is not enough to keep you alive)
163
Bundle branches from the Bundle of his go left and right allowing for what?
isovolumetric contractions (they also allow for the right ventricle / pulmonary valve to contract at a slightly different time than the left)
164
P Wave on an EKG indicates
Atrial Contraction
165
Where is the conduction pathway in the heart during atrial contraction?
from the SA node to the L/R atria to the AV node
166
Where is the conduction pathway in the heart during Ventricular contraction
bundle of his to the R/L bundle branches to the Purkinje fibers
167
QRS Wave on an EKG indicates
Ventricular Contraction
168
T Wave on an EKG represents...
Repolarization
169
ST Wave on an EKG represents
the beginning of relaxation after ventricular contraction
170
Isoelectric Line
imaginary horizontal line under the EKG
171
What does it mean if the ST wave (repolarization) drops below the isoelectric line?
It may be indicative of Ischemia in cardiac muscle tissue
172
What does it mean if the ST wave (repolarization) does not reach the isoelectric line?
It could indicate infarction (tissue death)
173
What can a peak T wave indicate?
Hyperkalemia
174
Hyperkalemia
too much Potassium (K+) in the blood
175
Depolarization
Activation - inside of the cell becomes less negatively charged due to a greater number of positive ions going into the cell
176
Repolarization
Deactivation - becomes more negative again as positive ions leave
177
Membrane Potential
Electrical (voltage) difference across the cell membrane that is related to changes in permeability of the membrane to sodium and potassium
178
Threshold of Fire
Depolarization - point at which the cell membrane's selective permeability to sodium and potassium is temporarily disrupted
179
Hyperpolarization
Resting membrane potential becomes more negative than it initially was
could be due to hypokalemia (low potassium)
180
The membrane pump ___ a passive process
is not
181
What is the ratio of Na pumped out to K pumped in generating the resting membrane potential?
3 Na are pumped out for 2 K in for every ATP expended
182
Level 4 is the resting membrane potential set by K... what is the voltage
-96 mV
183
What sets the threshold to fire?
calcium
184
Repolarization prevents ..
summation/Tetany - so many firings from occurring that the heart cannot pump
185
Absolute versus Relative Refractory Periods
these are periods of repolarization when another firing cannot occur yet
In absolute, the firing cannot occur at all and is near the initial drop on the diagram
In relative, this is the second half of the drop that could potentially get a strong enough signal to fire again before reaching rest
186
What can occur in a relative refractory period?
Arrhythmia
187
As heart rate increases, ____ decreases
Diastole (little filling can occur leading to disorientation from the brain not getting enough O2)
188
Increase in the heart rate leads to increased...
metabolic demand, O2 consumption, and glucose consumption
189
Normal Heart Rate
60-100 bpm
190
Sinus Tachycardia
> 100 bpm
191
Sinus Bradycardia
< 60 bpm
192
What does Sympathetic Stimulation from the ANS do to the heart?
Releases NEP --> increase heart rate, conduction speed through AV node, atrial and ventricular contractility, and peripheral vasoconstrition
193
When does Sympathetic stimulation occur?
when a decrease in pressure is detected
194
What does Parasympathetic Stimulation from the ANS do to the heart?
Releases Acetylcholine --> Decreases HR, lessens atrial and ventricular contractility and conductivity
195
When does Parasympathetic stimulation cocur?
When an increase in pressure is detected (vasodilation occurs to counteract it)
196
80% of NEP turns into...
EP
197
The only input for PNS on the cardiac system is through ...
the vagus nerve
198
ECG/EKG
Electrocardiogram
Common, noninvasive diagnostic test that evaluates heart function by recording electrical activity
can show ST depression and Peak T wave abnormalities
199
How to implement the ECG?
1. Determine whether the client can lie still, breath normally, and refrain from talking
2. Reassure them an electrical shock WILL NOT OCCUR
3. Document all their meds that may influence results
200
ECG P Wave represents
contraction of the atrial muscles / atrial depolarization
201
ECG QRS complex represents
Contraction of the ventricles / ventricular depolarization
This is when the conduction signal is moving through here
202
ECG T Wave represents
electrical changes during the relaxation phase of the ventricles / ventricular repolarization
203
Why can't we see Atrial repolarization on an ECG?
the QRS complex covers it up since it occurs at the same time
204
On an EKG we cannot see ...
the atrial "kick"
205
What can ST wave elevation indicate
infarction of cardiac tissues
206
What can ST wave depression indicate
hypoxia/ischemia/interrupted blood flow
207
What can a Peak T Wave indicate
too much potassium
208
Echocardiogram
Laboratory, noninvasive procedure using an ultrasound (most uncomfortable part is the gel)
Gel is applied to chest and a transducer is moved over the area to make an image of the internal heart structures like wall movement, valve opening and closing, and blood flow through
Can take 0.5 to 1.5 hours to do depending on type of echo needed
209
What does the echocardiogram evaluate?
How well the heart is moving
How well the valves are working
The size of the heart and its pumping chambers
How much blood when full and what was ejected from the ventricles
210
How to implement an Echocardiogram?
determine the client's ability to lie still, breath normally, and refrain from talking
211
Ejection Fraction
measure of how well the heart is performing as shown by the echocardiogram
It is found by taking the measure of volume in the ventricle when full and volume in ventricle after ejection
212
Exercise EKG
"Stress Test"
Exercise on equipment (most commonly treadmill) until ischemic ECG changes, angina, dyspnea, or SOB - occurs due to not enough O2 getting to myocardial cells thus triggering pain receptors
Noninvasive (invasive if used with radionuclide)
Studies heart during activity and detects coronary artery diseases
consent form needed due to potential complications
213
Exercise ECG should not be performed when ...
There is:
significant aortic stenosis
Untreated HTN
CHF
unstable angina
214
CHF stands for
Congestive Heart Failure
215
Significant Aortic Stenosis
Cannot open the aortic valve fully, thus leading to not being able to increase blood supply well, and thus could send someone into anginal attack with ECG changes
216
Unstable Angina
Pain in myocardial muscle tissue from unknown reasons
217
Persantine
for patients who cannot do exercise
it causes dilation of coronary exercise to make you feel like you exercised
218
What may be added during an exercise EKG?
Radionuclide studies (Thallium)
219
Bruce Protocol
Increasing the incline and speed of the stress test every 3 minutes until either target heart rate is reached with no issues or some other problem occurs
A cardiologist must be present for the test
220
What sort of patients get an Exercise EKG?
ones who are suspected of having heart disease or a blockage in order to better evaluate, so long as they have not had an MI
221
What to do Preprocedure for an Exercise Test?
Ensure informed Consent
Ensure client has adequate rest the night before
Instruct client to eat a light meal 1 to 2 hours before
Instruct client to avoid smoking, ROH, and caffeine prior to procedure
Ask physician about taking prescribed meds on day of procedure
Instruct client to wear nonconstructive, comfortable clothing and supportive shoes
222
What to do Postprocedure for an Exercise Test?
Instruct client to notify the physician if any chest pain, dizziness, or SOB occurs
Instruct client to avoid hot bath/shower for at least 1 to 2 hours post procedure (as it can cause vagus response)
223
Holter Monitoring
A noninvasive test where client wears a Holter monitor and an ECG tracing is recorded continuously over a period of 24 hours or more
Not used as much now that we use event monitors which are smaller, lightweight, and disposable
Its like a continuous ekg
224
What does a Holter Monitor do?
it takes an ECG tracing and can ID disrhythmias while evaluating the effectiveness of antidysrhythmics or pacemaker therapy
225
Implementation of Holter Monitoring
Instruct client to resume normal daily activities and to maintain a diary documenting activities and any symptoms that develop
226
Coronary Arteriography
An invasive cardiac catheterization that is the most precise means to document presence of CAD
It takes X-Rays of the heart and tells presence of CAD and measures LVF (Left ventricular function)
227
The gold standard of cardiac tests?
Coronary Arteriography / Coronary Catherization
228
When is a coronary arteriography indicated for patients?
Patients with:
Severe Angina
Recurrent Chest Pain of Uncertain Etiology
Survivors of Cardiac Arrest
Those suspected of CAD or an active MI
229
What measurements of left ventricular function (LVF) does a coronary arteriography give?
1. LVEDP (left ventricular end diastolic pressure)
2. LVEDV (left ventricular end diastolic volume)
3. Ejection Fraction (EF)
230
The coronary arteriography can detect coronary artery stenosis (narrowing). What percentage of occlusion is significant?
greater than 70%
when it is this high there is limited flow and a heparinized stent needs to be put in place to hold the coronary artery open
231
If someone is having an active heart attack, where do they need to go in a hospital and why?
They need to go to the cath lab immediately and have an occlusion opened in order to reperfuse the myocardium and prevent as much tissue death as there would have been
232
Occlusion on a Coronary Arteriography appears as ...
A space in a vessel with no coloring
233
Layers of the Blood Vessels
Tunica Adventitia
Tunica Media
Tunica Intima
234
Tunica Adventitia
Outermost vessel layer
connective tissue
prevents vessel from moving around
235
Tunica Media
Middle vessel layer
vascular smooth muscle
Has its tone controlled by the SNS which determines vasconstriction or dilation
236
Increased Tunica Media Tone leads to
Vasoconstriction
237
Decreased Tunica Media tone leads to
Vasodilation
238
What has little input on vasculature?
PNS
239
Tunica Intima
Innermost vessel layer
very smooth single layer of cells permitting laminar blood flow
continuous with the heart
has no stop gaps for debris to collect or clots to occur
240
Two types of Blood Vessesl
Resistance Vessels
| Capacitance Vessels
241
Resistance Vessels
Arteries and Arterioles
No Valves
Thick Muscular Walls
Work under high pressure, therefore no valves
242
Capacitance Vessesl
Veins and Venules
Has Valves
Elastic and Distensible
High Capacity to Hold Blood
243
At any time ___% (___L) of blood volume is in the arterial/resistance system, and ___% (__L) are in the venous/capacitance system
arterial - 25% (1.25 L)
venous - 75% (3.75L)
244
The pressure in the right atrium is ..
almost zero
245
SBP
Systolic BP
about 120 mmHg
Highest pressure achieved by contraction of L ventricle
246
DBP
Diastolic BP
about 80 mmHg
Blood pressure maintained in aorta between ejections
247
Which blood pressure permits a continuous forward flow of blood?
Diastolic Blood Pressure
248
Pulse Pressure
SBP - DBP = Pulse Pressure
About 40 mmHg
249
MABP
Mean Arterial Blood Pressure
An estimate reflecting average pressure during contraction and relaxation
Good indicator of tissue perfusion in critically ill patients
In premature infants, the MABP should match the gestational age
250
CO
Cardiac Output
CO = Stroke Volume (SV) TIMES HR (SVxHR=CO)
ex: CO = 70 mL/beat x 70 beat/min = 4900 mL/min (~5 L)
251
BP equation
BP = CP x TPR (Total Peripheral Resistance)
Could use Mean Arterial BP instead of TPR too
252
About how many L of blood is re-circulated every minute?
5 Liters (4900 mL or so)
253
SV
Stroke Volume
amount of blood ejected with each ventricular contraction
254
What is the mean Stroke Volume?
about 70 mL/beat
255
EDV
End Diastolic Volume
Total volume of blood in the left ventricle at the end of filling JUST PRIOR TO CONTRACTION
256
About how much volume does the L ventricle hold?
about 100 mL
257
What is the EDV a function of?
1. Venous return to R atrium
2. Strength of atrial contraction (kick) during ventricular filling
3. Amount of blood pumped out of ventricle during last contraction
258
ESV
End Systolic Volume
EDV - SV = ESV
Amount of blood left in heart after systole / after contraction
ex: EDV (100mL) - SV (70mL) = 30 mL ESV
259
EF
Ejection Fraction
Percent volume of blood ejected with each ventricular contraction (about 55-75% of total ventricular volume)
EF = (SV/EDV) = (70mL/100mL) = 70%
260
TPR
Total Peripheral Resistance (AKA: Systemic Vascular Resistance (SVR) or Peripheral Vascular Resistance (PVR))
Reflects the tone (Degree of vasoconstriction) of resistance vessels as well as the viscosity of the blood
261
Vasoconstriction ___ BP
Increases
262
Vasodilation ___ BP
Decreases
263
Aortic Impedence
Loss of elasticity of the aortic walls ("stiffening)
Increases with aging AND functioning of the aortic valve
common in people >80
Aortic Narrowing Occurs --> L Ventricle must generate higher pressure to get blood through --> Ventricle Hypertrophy may occur
264
Starling's Law
The force of a contraction is directly proportional to the initial length of the cardiac muscle fiber at onset of contraction
Myocardial fiber stretch has an upper optimal limit, and when exceeded, contraction strength decreases
(Basically, if more blood goes into the ventricle a harder contraction occurs but if it keeps occurring contraction strength is loss as cardiac muscles stretch out)
265
According to starling's law, the degree to which heart muscle is stretched corresponds to ...
EDV (end diastolic volume)
266
Preload
Degree of myocardial muscle stretch / How much blood is returned to the right atrium
So, Increased preload --> increased stretch --> increased force of ventricular contraction
Related to the degree of compliance (ability to stretch) of the ventricular wall
267
What things decrease compliance in the ventricular wall, leading to lower preload?
Ischemic heart muscle
Hypertrophied heart muscle
268
Heart Failure does what to compliance?
Increases stretching, but without increasing the force of ventricular contraction
269
Afterload
the pressure that the left ventricles has to push against (system pressure) - NOT amount of blood after contraction as that is ESV
The pressure the heart must overcome due to resistance of the aortic and pulmonic valves (aortic impedance)
Determined by the condition and tone of the aorta and resistance offered by systemic and pulmonary arterioles (TPR)
270
Things that increase Afterload and what is leads to
Aortic Stenosis / Hypertension --> Increased Afterload --> Increased Cardiac workload and increased O2 consumption
271
When myocardial contractility is increased...
More Blood is Ejected
Decrease in ESV
Increase in Systolic EF
272
When myocardial contractility is decreased...
Less blood is ejected
Increase in ESV
Decreased Systolic EF
273
The most important factor in ventricular performance is ...
MYOCARDIAL CONTRACTILITY
274
What influences ventricular performance and myocardial contractility?
Afterload
Preload
SNS Stimulation
275
What is myocardial contractility dependent on?
Concentration of catecholamines in the heart muscle, so EP and NEP directly stimulating Beta Adrenergic receptors in the myocardium to increase contraction force
276
Negative Iontropic Effects
Hypoxemia of Myocardium
Hypercapnia
Acidemia (Acidosis)
*All of these depress the myocardium
277
What regulates BP?
ANS (SNS and PNS)
278
The sympathetic nervous system uses ____ transmitters to ___ BP; The parasympathetic nervous system uses ___ transmitters to ___ BP
Adrenergic, Increase, Cholinergic, Decrease
279
EP and NEP are Positive ...
Inotropes
Chronotropes
Dromotropes
280
What receptors does NEP go to?
1. Beta 1 in the heart
2. Beta 2 in the lungs
3. Alpha 1 in Vascular Smooth muscle
4. Alpha 2 in the CNS
281
What nerve do PNS impulses travel on?
CN X (Vagus)
282
What does cholinergic signals do to the heart?
Decrease HR and Force of Contractions (slightly)
Its a negative chronotrope, inotrope, dromotrope
283
The cholinergic system has little control over...
blood vessels due to only one nerve pathway
284
What happens when beta 1 receptors receive NEP?
Increase HR and Increase Force of Contractions in the heart
285
What happens when beta 2 receptors receive NEP
bronchodilation of the lungs
286
What happens when alpha 1 receptors receive NEP?
vasoconstriction of the vascular smooth muscles
287
What happens when alpha 2 receptors receive NEP?
inhibition of CV center (where PNS works against things)
288
Baroreceptors
Work to sense BP changes
289
Where are important baroreceptors found?
1. carotid sinus to monitor Bp in the brain
| 2. Aortic Arch to monitor BP to the heart and make sure adequate blood flow gets to the brain
290
Most important function of baroreceptors...
to modify BP during postural changes or valsava maneuver
291
What do baroreceptors do exactly when change is detected?
Decreased BP --> Decreased Stimulation of Vasoconstriction and cardioinhibitory center to increase HR --> Increased CO and Increase BP
Increased BP --> Stimulation of vasodilation and cardioinhibitory center to decrease HR --> Decreased CO and Decreased BP
292
Chemoreceptors
Sensitive receptors to O2, CO2, and H+ in the blood in order to do their primary function of regulation of ventilation
293
Where are chemoreceptors located?
In the carotid bodies at bifurcation of common caoritds in aortic bodies of aorta
294
How do chemoreceptors communicate, and when are they stimulated?
They are stimulated when arterial pressure drops below a critical level, and they communicate with the vasomotor center and induce widespread vasoconstriction to increase arterial pressure
295
People with chronic lung disease may develop ___ and ___ ___ due to ____
systemic and pulmonary HTN d/t hypoxemia (related to chemoreceptors
296
What secretes NEP and EP into the blood?
Adrenal Medulla (DUAL-LA)
297
NEP and EP produce ____ chronotropic and inotropic responses
Positive
298
NEP and EP hormones travel to the ___
heart
299
When is the RAA system initiated?
when kidneys sense low pressure, and thus stimulate the SNS
Decreased Pressure in Renal Arteries --> Decreased Na in Renal Tubules --> SNS Stimulation
300
What is the response to RAA initiation?
Juxtaglomerular cells secrete renin --> Renin turns angiotensinogen into angiotensin I --> Angiotensin I converted to Angiotensin II by ACE in the lungs --> Vasoconstriction occurs --> BP and Aldosterone levels increase --> Na and H2O retention by kidneys increase ---> ECF Volume increases --> Increased BP
301
How can RAA make heart failure worse?
The system increases volume and pressure when it drops which is supposed to compensate, but in this case causes increased volume and pressure leading to increased workload for an already struggling heart
302
ADH
Antidiuretic Hormone / Vasopressin
Released when Plasma Osmolarity increases (blood is viscous) or BP decreases
potent vasoconstrictor
303
What is the response to increased plasma osmolarity or decreased BP?
Posterior pituitary secretes ADH --> ADH directs water in the collecting ducts of the kidney --> Plasma volume increases --> BP and CO increase
304
Angiotensin II is a potent ___
vasoconstrictor
305
ADH is a potent ___
vasoconstrictor
306
Atrial Stretch Receptors and ANP
ANP - Atrial Natriuretic Peptide / Factor
These two things react to the degree of distension of the Left Arterial walls during diastole
307
Problem and Response of Atrial Stretch Receptors
Increased Venous Return (Increased BP) --> Increased heart firing rate --> ANP release stimulated from atrial walls --> renal arterioles vasodilate --> glomerular filtration rate increases --> aldosterone inhibited by increased urinary Na loss --> inhibits ADH release from posterior pituitary causing diuresis --> decreased blood volume and BP
308
What does ANP effect?
It directs the kidney to get rid of sodium and the water follows it
309
BNP
Brain Natriuretic Peptide
Released from ventricles in response to stimulus from ventricular stretch receptors
Opposes RAA activity and is MUCH stronger than ANP's effect
310
BNP correlates to ...
Left Ventricular Pressure
311
How does BNP oppose RAA activity?
1. Vasorelaxation
2. Inhibition of aldosterone secretion from adrenal gland and renin from the kidney
3. Increased natriuresis and reduction in blood volume
312
Natriuretic means ...
opposes sodium
ex: BNP is a hormone opposing sodium and telling the body to rid of it
313
____ is a good marker for heart failure with 300 picograms/mL indicating ___ heart failure, 900 picograms/mL indicating ___ heart failure, and 0.5 to 50 picograms/mL indicating ___ heart failure
BNP, mild, severe, no
314
Blood pressure is a function of the ___ of the blood vessels
tone
315
Essential Hypertension
Idiopathic (Don't Know Why) HTN
Most common cardiovascular disorder
Primary (90%) and Secondary (<10%)
316
What is the blood pressure reading on someone with essential HTN?
>140 SYS OR >90 DIAS
317
Essential hypertension is a strong risk factor for ...
Heart disease (#1), Stroke (#3) and CRF (chronic renal failure)
318
What is the number 1 killer?
HTN (as it causes heart disease) leading to more than 30,000 deaths per year in the US
319
What is the prevalence of Essential HTN
60 million (20-25% of US population) and it increases with age
320
When does essential HTN onset occur?
Males > Females
20s-30s
African Americans x2 more likely than Whites
321
What are some risk factors increasing essential HTN chance?
Some modifiable and some not:
1. Family History (2x more likely with one)
2. Age (Increase with age)
3. Race (more prevalent and severe in A Americans
4. Obesity (2x more prevalent; especially in apple shape)
5. Stress (increase BP with pain and family crisis, decrease BP with sleep and rest)
6. Alcohol (more than 3 drinks a day)
7. Oral Contraceptives (women over 35 and smoking at greatest risk)
8. Na Intake (plays a part in some people's HTN, and its role is unclear as a decrease does not necessarily mean decrease in BP)
322
What body shape is at higher risk of HTN?
Apple body shape (Pear shape is okay because ab fat is active fat)
323
Manifestations of Essential Hypertension
- usually asymptomatic ( a silent killer)
complicates detection and treatment
Headache in a small # of patients upon awakening in occipital and neck areas
Nocturia (common early symptom indicating kidney losing ability to concentrate urine)
Ophthalmoscope will show retinal vascular narrowing, AV nicking, hemorrhages, exudates, papilledema (optic disk swelling - emergency as it means brain swelling)
324
Diagnosis of Essential Hypertension
At least 3 BP measurements on 3 Different Occasions when it exceeds 90 DIAs or 140 SYS
BP must be taken when rested for at least 5 minutes, they have not smoked or had caffeine in the last half hour, and with a properly sized BP cuff
325
Optimal Blood Pressure
< 120 sys AND <80 DIAS
326
Normal Blood Pressure
< 130 sys AND < 85 DIAS
327
High Normal Blood Pressure
130-139 sys OR 85-89 DIAS
328
Stage 1 - Mild HTN Blood Pressure
140-159 sys OR 90-99 DIAS
329
Stage 2 - Moderate HTN Blood Pressure
160-179 sys OR 100-109 DIAS
330
Stage 3 - Severe HTN Blood Pressure
Greater than or Equal to 180 sys OR greater than or equal to 110 DIAS
331
HTN in infancy is usually due to ...
something different than in people 6+ (typically renal parenchymal disease)
332
Most Adolescent and Adult HTN is due to ..
Essential Hypertension
333
ISH
Isolated Systolic Hypertension
HTN in the Elderly
Stiffened arteries --> vessels without contractility during systole --> Increased systolic BP, decreased baroreceptor sensitivity, increase TPR, decreased renal blood flow
334
BP in ISH
>160 sys AND <90 Dias
335
Complications of ISH
2x-5x increased risk of CV death (from AMI and CHF)
2x-3x increased risk of stroke (from TIA and CVA)
ISH must be treated to stop heart failure
336
Secondary Hypertension
A type of essential hypertension that is NOT idiopathic ( a cause is known)
5-10% of HTN cases are this kind
337
What may cause Secondary HTN
Renal Disease
Endocrine Disorders
Vascular Disorders
Chemicals / Medication
338
Malignant Hypertension
DIASTOLIC BP above 120 mmHg
Is a medical emergency
A disease more prevalent in younger people (especially A American males, PIH, and those with renal disease)
It gives you a high risk of stroke
339
Response/Manifestation of Malignant Hypertension
1. AMI
2. Renal Failure
3. Intense cerebral arterial spasm to protect brain from excess pressure and flow --> cerebral edema and optic nerve swelling occurs --> HTN, Encephalopathy, headache, restlessness, confusion, motor/sensory deficits, visual disturbances
4. can cause an emergency if anesthesia is taken with it present
340
TOD
Target Organ Disease
HTN Progression can lead to this
Diseases of various organs (cardiac, arterioles, kidneys, etc) brought on by HTN progression
341
Cardiac TOD
Increased L Ventricle Workload --> hypertrophy and increased O2 demand --> heart failure
342
Why are coronary artery disease and HTN so dangerous together?
There is a decreased O2 supply with a larger O2 demand
343
Arterioles TOD
smooth muscle hypertrophies --> decreased lumen diameter --> accelerates atherosclerosis
344
Kidney TOD
Hypertrophy and sclerosis of arterioles and glomeruli --> decreased GFR --> abnormal concentrating/ diluting mechanisms --> nocturia, proteinuria, microscopic hematuria, CRF, urine with same tenacity as blood if the loop of henle is broken (isosthenuria)
345
Examples of Other TOD
Aortic Aneurysm
Retinopathy
Cerebrovascular Diseaese
346
Treatments for Hypertension are ___ Modifications
Lifestyle
347
Lifestyle modifications to treat HTN
1. Weight reduction to decrease heart work load (want to drop about 15%)
2. Regular physical activity to lower resting HR and lower TPR
3. Decrease alcohol intake
4. Cease Smoking
5. Decrease sodium and fat intake while increasing calcium, potassium, magnesium in diet
6. Use Relaxation techniques to decrease resting HR and lower TPR
