Cardiovascular System Flashcards
(228 cards)
1
Q
What are the four parts of an electrocardiogram and what do they mean?
A
P wave is the depolarization of the atria
QRS complex is the depolarization of the ventricles
T wave is the repolarization of the ventricles
U wave is not completely know but is likely the repolarization of the papillary muscle
2
Q
What is isovolumic ventricular contraction?
A
This begins with the closure of the mitral valve (generates the first heart sound). The blood volume is the end-diastolic volume and the ventricles are beginning to contract
3
Q
What is ventricular ejection?
A
This begins with the opening of the semilunar valve due to an increase in ventricular pressure. The blood is ejected from the ventricle. This ends with the closure of the semilunar valve
4
Q
What is isovolumic ventricular relaxation?
A
This begins with the closure of the semilunar valve (2nd heart sound). The blood volume in the ventricle is the end-systolic volume. The ventricle is relaxing
5
Q
What is ventricular filling?
A
This begins with the opening of the mitral valve due to the low ventricular pressure. Passive filling occurs and is followed by active filling due to the contraction of the atria
6
Q
What is the ventricular pressure volume loop?
A
A plot which is generated by plotting ventricular pressure against ventricular volume. It showcases the dynamic changes during one cardiac cycle
7
Q
What is the equation for cardiac output?
A
CO = HR x SV
8
Q
What is stroke volume?
A
The amount of blood pumped out of the ventricle per beat
9
Q
What is cardiac output?
A
The output of the heart per unit time
10
Q
What is cardiac index?
A
The cardiac output per body surface area. This is used to minimize the influence of body size on cardiac output
11
Q
What impact does increasing heart rate have on stroke volume and cardiac output?
A
Increasing the heart rate will decrease the stroke volume and increase the cardiac output (to a point, eventually cardiac output will decrease)
12
Q
Why does exercising cause CO and HR to increase so much?
A
Reduction of peripheral vascular resistance, positive inotropic effect to the contractile myocytes by an increase in sympathetic activity, and compressing action of the skeletal muscles with the venous valves to enhance venous return
13
Q
How do you calculate stroke volume?
A
SV= EDV - ESV
14
Q
What can impact stroke volume?
A
Preload, afterload, and contracitilty
HR can have an effect also, but it is much smaller
15
Q
How does preload impact SV?
A
Increasing preload will increase SV
16
Q
What impacts preload?
A
The degree of stretching of cardiac myocytes prior to contraction
17
Q
What is the formula for compliance?
A
Change in volume/ Change in pressure
18
Q
What do high and low compliance mean?
A
High compliance means the heart can be easily stretched during diastole
Low compliance means the heart will resist expansion during diastole
19
Q
How does compliance relate to end-diastolic pressure-volume relationship?
A
It is the inverse of the slope
20
Q
How does ventricular dilation impact EDV and EDP?
A
There is an increase in ventricular compliance so the ventricle can have an increased EDV without a large impact on the EDP
21
Q
How does ventricular hypertrophy impact EDV and EDP?
A
There is a decrease in ventricular compliance with causes an increase in the EDP for a given EDV
22
Q
What does an increase in venous return cause?
A
An increase in ventricular filling, so an increase in preload. This will increase EDP for a given heart.
23
Q
What does the Frank-Starling mechanism explain?
A
The phenomena through which an increase in preload creates and increase in the force of contraction of the heart
24
Q
What is the purpose of the Frank-Starling mechanism?
A
To ensure the outputs of both ventricles are matched so there is no shift in blood between the pulmonary and systemic circulations
25
What will an increase in venous return cause with respect to ESV?
The SV and CO will increase, but there will be no change in the ESV
26
What happens if an increase in SV due to an increase in VR changes the contractility status of the heart?
A decrease in ESV would occur
27
What is the length-tension relationship of the ventricle?
The relationship between changes of the initial length of a myocyte to the contractile force developed by the heart muscle
28
What does increasing the preload do to the force?
Increasing the preload increases the tension developed, which increases the velocity of tension development, and increases the force
29
What is the afterload?
The ventricular wall tension developed during ventricular ejection.
30
Ventricular wall stress can be estimated using what?
Laplace's law for a sphere
| Wall stress = (Intraventricular pressure x preload)/2(Wall thickness)
31
How is ventricular hypertrophy an adaptive mechanism?
To offset the increase in wall sress
32
What occurs in congestiv eheart failure?
The Frank-Starling mechanism fails to compensate for the increase in preload due to the decrease in contractile function
33
How does an increase in afterload impact the pressure needed?
A much higher pressure is needed to eject the same volume of blood
34
How does an increase in afterload impact SV?
Decreases the velocity of fibre shortening which results in a decrease in SV
35
What is the Y-intercept of a force-velocity relationship curve?
The maximum velocity that can be achieved by the muscle fiber in the absence of any load
36
What is the X-intercept of a force-relationship velocity curve?
The maximum force that the heart can generate at a given preload condition
37
How do changes in afterload impact preload?
When afterload increases the ventricle has to generate higher pressure to open the aortic valve. This decreases ejection velocity and increases ESV. This will cause an increase in EDV, and a decrease in SV.
38
What is contractility?
The property of contractile myocytes that account for the strength of contraction
39
How can ventricular EDP be used to evaluate cardiac performance?
Inadequate systolic emptying will increase ESV, which will increase EDV, which will increase EDP
40
How does stroke volume change in relation to a hearts contractility when EDV and EDP are increased?
The heart with the stronger contractility will have a larger increase in stroke volume
41
How does an increase in preload effect the stroke volume of a failing heart?
It has minimal impact because a failing heart already has a much higher EDP at a given stroke volume
42
In the case of ventricular hypertrophy, what does a small increase in EDV cause?
A large increase in EDP due to the low ventricular compliance of the heart
43
How does an increase in contractility impact cardiac index?
An increase in contractility increases SV and in turn generates a higher cardiac index
44
How can stroke volume be used to measure cardiac performace?
The higher the SV at a given preload that shorter the fiber lengths and smaller the ventricular chamber size.
45
What is the ejection fraction?
The fraction of the EDV ejected from the ventricle during each systolic contraction
46
What is the equation for ejection fraction?
EF = SV/EDV
47
When is ventricular pressure usually the highest?
Just before the opening of the semilunar valves
48
What is the Treppe phenomenon (Bowditch effect)?
Increase in heart rate reduces the time for Na-K ATPase to restore the concentration gradient which increases the amount of sodium in the cytosolic space. This inhibits Na-Ca exchanger activities and increases the Ca in the cytosolic space. This causes an increase in myocardial contractility
49
How will an increase in intropy impact the ESPVR?
ESPVR will move upward and to the left. It will also have a steeper slope
50
What is the best indicator of contractility?
Vmax
51
How will Vmax change if contractility is increased?
It will cause a parallel shift up and to the right
52
What is aortic stenosis?
Narrow opening of the aortic valve
53
What does the increase velocity of blood associated with aortic stenosis cause?
Turbulent flow which generates a systolic murmur
54
What does aortic stenosis cause in respect to cardiac output?
An increase in LVP, which causes and increase in afterload, which causes an increase in ESV and a decrease in stroke volume and cardiac output
55
What is mitral stenosis?
Improper opening of the mitral valve
56
What does resistance to flow due to mitral stenosis cause in the atrium?
Elevation of left atrial pressure
57
What contributes to incomplete ventricular fillinf?
Elevation of left atrial pressure (retention of blood in the atrium) and a decrease in EDV due to reduced venous return
58
What do the higher velocities of blood flow cause in mitral stenosis?
A diastolic murmur between S2 and S1
59
What is aortic insufficiency?
Incomplete closure of the aortic valve which allows for movement of blood between the aorta and the left ventricle at all times
60
How is stroke volume impacted by aortic insufficiency?
Preload increases which increases the peak systolic pressure. EDV and EDP are also increased which augment the increase in force of contraction which leads to an increase in SV.
61
What causes a diastolic murmur to be heard with aortic insufficiency?
Regurgitation during ventricular diastole
62
What is mitral insufficiency?
Incomplete closure of the mitral valve. This allows blood flow between the atrium and the ventricle constantly
63
What causes a systolic murmur in mitral insufficiency?
The back flow of blood during ventricular systole
64
What causes the rise in LAP during ventricular systole with mitral insufficiency?
Regurgitation of blood from the ventricle back to the atrium
65
How do EDV and ESV change with mitral insufficiency and why?
EDV is increased due to the increase in LV filling with the increase in LAP
ESV decreases because blood from the ventricle is regurgitated back to the LA during systole
66
What is physiological ventricular hypertrophy (Concentric hypertrophy)?
An adapting change to stress in order to enhance pumping capacity of the heart
This is reversible and non-pathological
67
What is afterload related pathological ventricular hypertrophy?
Induced by chronic increase in afterload, so the ventricle needs to generate a greater pressure chronically to eject the blood
68
What can afterload related pathological ventricular hypertrophy lead to?
Reduction in SV and elevation in ESP
| Can cause diastolic dysfunction and heart failure
69
What is preload related pathological ventricular hypertrophy (eccentric hypertrophy)?
An increase in ventricular wall stress caused by volume overload. This causes systolic dysfunction
70
What does preload related pathological ventricular hypertrophy cause?
A huge increase in ESV and EDV with minimal changes in EDP due to the high compliance. SV is decreased
71
What are the two pacemakers and what are their rates?
Sinoatrial node which beats at around 70-80 BPM
| The atrioventricular node which beats at around 40-60 BPM
72
What are pacemaker cells responsible for?
The genesis of automaticity leading to cardiac muscle contraction
73
What is autorhythmicity?
The combination of both the automaticity and rhythmicity properties. Automaticity is the ability of the cell to initiate its own pacemaking
Rhythmicity is the ability of a cell to maintain the regularity of pacemaking activity
74
In the ionic basis of automaticity what is phase 4?
It is initiated by the slow leak of Na and followed by Ca influx
75
In the ionic basis of automaticity what is phase 0?
It is the depolarization with calcium influx through the long-lasting voltage-gated channels after reaching threshold
76
In the ionic basis of automaticity what is phase 3?
Repolarization accomplished by rapid potassium efflux
77
What are the three variables that can influence cardiac rhythmicity?
Rate of diastolic depolarization, maximum diastolic potential, and threshold potential
78
What are the three regions of the AV node and how do they impact ventricular filling?
Atrionodal region, nodal region, and nodal-His
The atrionodal and nodal regions are the principle delay between atrial and ventricular contraction. This ensures ventricular filling
79
Where is the atrioventricular bundle and where does it go?
Located below the AV node and passes through the fibrous ring that separates the atria and the ventricles. It reaches the inter-ventricular septum to form two separated branches
80
Where are the bundle branches and how to they impact the depolarization?
A continuation of the AV bundle which is divided into left and right. The right bundle is considerably longer and thinner than the left bundle branch, which allows for septal depolarization from left to right
81
What are the Purkinje fibers and what is their job?
Inferior terminal branches of the bundle branches which have the fastest rate of conduction. They enable rapid, organized, and near synchronous depolarization and contraction of the ventricles
82
What are James fibers?
Fibers from the atrial inter-nodal tracts that pass around the AV node and enter the inter-ventricular septum.
83
What problems are associated with James fibers?
Pre-excitation can occur, which means the signals are not coming from the AV node and there is no delay for ventricular filling
84
What is paroxysmal?
The sudden onset of rapid or abnormal rhythms
85
What are Mahaim fibers?
Any direct connections between AV node, bundle of His, or bundle branches into the interventricular septum
86
What is the bundle of Kent?
A muscular bundle forming a direct connection between atrial and ventricular myocardium
87
What is the bundle of Kent capable of doing?
It can take the action potential back to the atrium, so one signal from the SA node can cause two heart beats
88
What is an electrocardiogram?
A graphic recording of the biopotentials generated by the myocardium during the cardiac cycle
89
How do the lengths of systole and diastole compare in a regular cardiac cycle?
Systole is shorter than diastole
90
What is the paper speed, square time, and square amplitude in a regular ECG?
The paper speed is 25mm/sec so each square is 0.04 seconds. One square of amplitude is equal to 0.1mV
91
What is the PR interval?
From the start of atrial depolarization (P wave) to the start of ventricular depolarization (R wave)
The time required for the depolarization wave from the SA node to spread through the right atrium and the duration of atrial contraction
92
What is the PR segment?
The end of atrial depolarization (P wave) to the start of ventricular depolarization (R wave)
This is the length of time of delay for the action potential passing through the AV node
93
What is the QRS duration?
From the beginning of the Q wave to the end of the S wave. This is the duration of ventricular depolarization.
94
What is the ST segment?
The end of ventricular depolarization (S wave) to the beginning of ventricular repolarization (T wave)
This is also known as the isoelectric line and it should be flat
95
What is the QT interval?
The beginning of ventricular depolarization (Q wave) to the end of ventricular repolarization (T wave)
This is the duration of ventricular action potentials and is correlated with heart rate
96
What is indicated by an abnormal PR interval?
A short PR interval could indicate Wolff-Parkinson-White Syndrome
A long PR interval could indicate a heart block
97
What is indicated by an abnormal QRS complex?
A wide QRS complex could mean a bundle branch block
| A tall QRS complex could mean ventricular hypertrophy
98
What is indicated by an abnormal ST segment?
Elevation could indicate epicardial ischemia
| Depression could indicate endocardial ischemia
99
What is indicated by an abnormal T wave?
An inverted T wave could indicate myocardial ischemia, intraventricular conduction delay, or an anxiety attack
100
Which limbs of an ECG are bipolar and which are unipolar?
Leads 1-3 are bipolar
| Leads aVR, aVL, aVF, and V1-V6 are unipolar
101
Where do the bipolar leads connect?
Lead one has the negative at the right arm and the positive at the left arm
Lead two has the negative at the right arm and the positive at the left leg
Lead three has the negative at the left arm and the positive at the left leg
102
What is overdrive suppression?
Pacemaker cells with higher intrinsic rhythm prevent all latent pacemakers in the heart from firing
103
How does heart tissue become hyperpolarized and what can this cause?
Heart cells become more negative from the Na-K ATPase pump working. This means it takes a longer time for the current to reach threshold, so automaticity is slowed.
104
What is the phenomenon of the re-entry loop?
Cardiac impulses may re-excite the myocytes through which it had passed previously within the same cardiac cycle
105
What are the three conditions required for re-entry to occur?
Closed conduction loop, unidirectional block, and sufficiently slow conduction around the loop
106
What is a sinus rhythm?
SA node controls the cardiac rhythm
107
What is sinus bradycardia?
Sinus rhythm with a rate less than 60 BPM
108
What is sinus tachycardia?
Sinus rhythm with a greater than 100 BPM
109
What is arrythmia?
Onset of abnormal heart rhythms
110
What is escape rhythm?
Prolonged impairment of SA node allows latent pacemaker to initiate an escape beat
111
What is an escape rhythm?
A situation when SA node has a lower automaticity than that of the AV node
112
What is an ectopic beat?
Any heart beat generated by impulse other than the one from SA node
113
Why does the impulse from latent pacemakers travel in two directions?
The AV node is in between the atrium and ventricles. An impulse travels towards the ventricles and towards the atrium, which leads to an inverted P wave
114
What is a ventricular escape rhythm?
Conduction blockage of the AV allows bundle of His or bundle branches to become latent pacemaker
115
What is ventricular tachycardia?
High heart rate (usually over 120) with a wide QRS complex
116
What is ventricular flutter?
A very high heart rate (over 200BPM) but a lowered cardiac output
117
What is ventricular fibrillation?
Nonfunctional muscle contraction (quivering) which produces 0 cardiac output
118
What is heart block?
Impaired conduction through the AV conduction system
119
What is a first-degree AV block?
There is an increased delay between atrial and ventricular depolarization. The PR interval is longer
120
What is a Mobitz 1 second-degree AV block?
The PR interval progressively lengthens until a QRS complex is absent. After the absence it continues to repeat.
121
What is the Mobitz 2 second-degree block?
There is no gradual lengthening of PR intervals, but occasionally QRS complexes will disappear
122
What is a third degree AV block?
Complete heart block with complete failure of conduction between the atria and ventricles
123
What occurs if there is a right bundle branch block?
There is normal conduction down the left bundle branch and the right ventricle is depolarized via gap junctions
124
What occurs if there is a left bundle branch block?
Occurs when transmission of impulses does not reach the left ventricle. The left ventricle is depolarized via gap junctions
125
What is hemodynamics?
The study of the fluid mechanics of blood
126
What is the A wave of atrial pressure?
The rising phase occurs due to atrial systole after the rapid ventricular filling phase
127
What is the C wave of atrial pressure?
The closure of the tricuspid valve while atrial filling continues
128
What is the region between the a and c waves in atrial filling?
The end of active ventricular filling (atrial relaxation)
129
What is the V wave of atrial pressure?
The filling of the atrium after it is fully stretched
130
What is pulmonary wedge pressure used for?
To estimate atrial pressure
131
What do you use to measure pulmonary wedge pressure?
Swan-Ganz catheter
132
What causes changes in blood velocity?
The diameter of the vessel
133
Which region of the cardiovascular system has the largest cross sectional area?
The capillaries
134
What is hydraulic resistance?
The changes in pressure divided by flow rate
135
What is the dominant factor in determining resistance to flow?
The radius of the vessels
136
How are the branches of the vascular system arranged?
Parallel to eachother
137
What is the primary resistance vessel?
Arterioles
138
What innervates the resistance vessels?
Autonomic nerves
139
What is used to predict the flow pattern?
Reynolds number
| Re=pQD/uA
140
What does a flow pattern less than 2000 or more than 3000 mean?
Less than 2000 means laminar flow and more than 3000 means turbulent flow
141
What is the flow rate proportional to in laminar flow?
Pressure drop
142
What is flow rate proportional to in turbulent flow?
The square root of pressure drop
143
What is hematocrit?
The ratio of volume of red blood cells to volume of whole blood
144
Why do arteries have a tendency to collapse?
Due to the elastic property of the elastic and collagen fibers enclosing the artery
Due to active tension by vascular smooth muscle cells
145
What is the critical closing pressure for a given blood vessel?
The mean blood pressure at or below which the blood vessel will collapse
146
What is the effective circulating volume?
The blood volume within the vasculature that can be utilized to perfuse the organ systems within our body
147
What is blood pressure?
The force exerted by blood against a vessel wall
148
What is peripheral vascular resistance?
The diameter of the small arteries and arterioles which contributes to the resistance to flow between the arterial and venous compartments
149
What is the equation for systemic vascular resistance?
SVR= (MAP- CVP)/CO
MAP is mean arterial pressure
CVP is central venous pressure
150
What is systolic pressure?
The upper limit of the periodic oscillations of blood pressure initiated by the ventricular systole
Usually around 120mmHg
151
What is diastolic pressure?
The minimum pressure within the arteries during ventricular diastole
Usually around 80mmHg
152
What is pulse pressure?
The difference between systolic and diastolic pressure
153
What is mean arterial pressure?
The average pressure in the arteries over time
| Calculated by 1/3 SP + 2/3 DP
154
What are high pressure baroreceptors?
The primary sensors for the detection of arterial blood pressure changes
155
Where are high pressure baroreceptors located?
The carotid sinus and the aortic arch
156
What impact do high pressure baroreceptors have?
They are stretch receptors that when fired cause inhibitory sympathetic effects and excitatory parasympathetic effects to result in lowered blood pressure and heart rate
157
Where are low pressure baroreceptors located?
Venoatrial junctions, cardiopulmonary, and low pressure chambers of the heart
158
What do type A fibers of atrial baroreceptors do?
Fire during atrial depolarization to monitor heart rate
159
What do type B fibers of atrial baroreceptors do?
Fire during ventricular systole for the monitoring of atrial volume
160
What does the bainbridge refelx do?
Increase in stretching of the B fibers increases HR when baseline HR is low. This acts as a counterbalance to the high pressure baroreceptors when increase firing of the high pressure baroreceptors causes a decrease in HR
161
What do chemoreceptors detect?
Changes in PO2, PCO2, and H concentrations
162
What is the primary function of chemoreceptors?
To regulate respiratory activity and to maintain the blood gas level within a narrow physiological range
163
What can cardiovascular function be controlled by?
Blood pressure and blood volume
164
What are the two categories of cardiovascular function control?
Neural and humoral
165
What are the three levels of neural control of cardiovascular function?
Cortex, hypothalamus, and the medulla
166
What is the cortex responsible for in neural control of cardiovascular function?
Altering cardiovascular function during emotional stress
167
What is the hypothalamus responsible for in neural control of cardiovascular function?
Modulating medullary neuronal activity
168
Why is the resting heart rate lower than the intrinsic firing rate of the SA node?
Parasympathetic nuclei are tonically active
169
What does vagal stimulation causing the release of acetylcholine cause?
Negative chronotropy, dromotropy, and inotropy
170
Where are the negative inotropic effects due to parasympathetic innervation more evident?
The atria
171
Where do the right and left vagus nerves innervate during parasympathetic innervation?
The right innervates the SA node
| The left innervates the AV node and the ventricular conduction systems
172
What does stimulation of sympathetic innervation do to cardiovascular function?
Causes tachycardia and vasoconstriction
173
What does sympathetic innervation and norepinephrine release cause?
Increase in chronotropy, dromotropy, and inotropy
174
What causes transient coronary vasoconstriction?
Sympathetic stimulation of the heart
175
What is the primary variable that needs to be regulated to control cardiovascular function?
Systemic arterial blood pressure
176
Where do catecholamines come from and what activates their release?
The adrenal medulla
| Activated by the preganglionic sympathetic nerves during times of stress
177
What occurs humorally when epinephrine is present in low levels?
Vasodilation due to the greater affinity for B2 receptors
178
What occurs humorally when epinephrine is present in low to moderate levels?
Increase in heart rate, contractility, and conduction velocity
179
What are the three basic mechanisms by which epinephrine increases blood pressure?
Direct stimulation of myocytes in ventricles, increase in heart rate, and vasoconstriction in resistance vessels and veins
180
What is norepinephrine an agonist of?
B1 and a
181
What does norepinephrine cause in the heart?
Increase in systolic and diastolic pressure. Increase in peripheral resistance
Increase and then decrease in HR
182
What is epinephrine an agonist of?
B1, B2, and a
183
What does epinephrine increase in the heart?
HR, CO, and SV due to B1 activation
184
What is isoproterenol an agonist of?
Non-specific B agonist
185
What occurs humorally when epinephrine is present in high levels?
Increase in cardiac output and systemic vascular resistance
186
What does the renin-angiotensin-aldosterone system cause?
Increased blood pressure and blood volume
187
What does the atrial natriuretic peptide cause?
Decreased blood pressure and volume
188
What does vasopressin cause?
Increase in blood pressure and blood volume
189
What is ventricular end diastolic volume a function of?
Ventricular filling pressure, ventricular filling time, and ventricular compliance
190
How will an increase in the rate of output impact atrial pressure?
Right atrial pressure will decrease
| If flow continues to increase, pressure will drop to a negative value
191
What causes the plateau phase in the vascular function curve?
The negative right atrial pressure
192
What happens when cardiac output is zero?
The veins are closing. This is the mean systemic filing pressure, which is also the closing pressure
193
What is mean systemic filling pressure a function of?
Fluid volume (directly) and overall compliance (inversely)
194
What is central venous pressure?
The blood pressure in the thoracic vena cava in the proximity of the right atrium
195
What is the equation for venous compliance?
C=V/P
C is Compliance
V is change in blood volume
P is change in CVP
196
What does the vascular function curve describe?
The relationship between CVP and CO
197
How does transfusion impact CVP?
It increases, because blood volume is higher
198
How does hemorrhage impact CVP?
It lowers it, because blood volume is lower
199
How does vasodilation impact CVP?
It increases it, because venous blood volume increases due to decreased resistance
200
How does vasoconstriction impact CVP?
It lowers it, because venous blood volume decreases due to increased resistance
201
How does increasing sympathetic stimulation impact CVP?
It will decrease due to the increase in CO
202
How does increasing peripheral resistance impact CO and CVP?
CVP remains relatively unchanged (lowered volume and constricted vessels counterbalance)
CO decreases
203
How does heart failure impact CO and CVP?
CO decreases so CVP increases
204
How does hypervolemia impact CO and CVP?
CO increases due to increased preload
| CVP increases due to increased blood volume
205
How much of the body weight is blood?
7-8%
206
How much of the blood volume is cellular component?
Around 45%
207
How much more numerous are erythrocytes than white blood cells and platelets?
700x more than WBC
| 17x more than platelets
208
What is the bone marrow broken up to produce and in which ratios?
25% red blood cells and 75% white blood cells
209
Why is the concentration of red blood cells so much higher than that of white blood cells in the blood?
White blood cells often have a shorter life span and they undergo transendothelial migration, leaving the blood
210
How much of the plasma is water?
92%
211
What are the major plasma proteins?
Albumins, fibrinogen, globulins, and coagulation factors
212
What is hemostasis?
Arrest of bleeding or prevention of hemorrhage
213
What occurs in the vascular phase of hemostasis?
Contraction of vascular smooth muscle cells within the damaged vessel
214
What happens neurally during the vascular phase of hemostasis?
Increase in sympathetic tone to cause vasoconstriction
215
What happens chemically during the vascular phase of hemostasis?
Chemical byproducts of activated platelets and coagulation promotes vasoconstriction
216
What occurs during platelet adhesion?
Platelets bind to themselves or to other components
217
What occurs during platelet activation?
Platelets undergo exocytosis of their storage granules. This causes amplification of the platelet activation response
218
What occurs during platelet aggregation?
They form molecular bridges between platelets and subendothelial structures such as collagen and fibrinogen
219
What is the end result of platelet adhesion, activation, and aggregation?
The formation of a platelet plug
220
What is coagulation?
The process of blood clot formation
221
What are blood clots made of?
Mesh of fibrin containing blood cells and serum
222
What activates the intrinsic pathway of coagulation?
Tissue factors released by the damaged tissue
223
What activates the intrinsic pathway of coagulation?
Factor 12 coming in contact with damaged blood vessels
224
What is necessary for coagulation?
A functional liver and vitamin K
225
What is fibrinolysis?
Degradation of fibrin which holds together the blood clot
226
What does tissue plasminogen activator do?
It is an enzyme produced by damaged endothelial cells which catalyzes the conversion of plasminogen into plasmin
227
What is streptokinase?
A product of the beta hemolytic streptococcus that can be used as a fibrinolytic agent
228
What is urokinase?
A protease expressed by the plasminogen activator urokinase gene that is involved in degradation of the extracellular matrix
