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Unit 3 Flashcards

1
Q

Cardiac output is determined mainly by

A

Venous return

CO= VR (Also CO = SV X HR)

SV = stoke volume
HR = heart rate
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2
Q

Factors that influence VR

A

Body metabolism (local flow and autoregulation) - VR is a summation of all local blood flows

Age

Body size

Gender (heart size)

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3
Q

Factors affecting heart rate

A

Autonomic innervation
Hormones
Fitness levels
Age

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4
Q

Factors affecting stroke volume

A 
Heart size
Fitness levels
Gender
Contractility
Duration of contraction
Preload (EVD)
Afterload (resistance)
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5
Q

Stroke volume =

A

SV = EVD - ESV

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6
Q

Cardiac index increases from age ___-___

It decreases after age

A

0 - 10ish

10ish

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7
Q

CO will match VR via the following mechanisms:

A 
Frank sterling’s mechanism (effects force of contraction)
Bainbridge Reflex (effects rate of contraction)
SA node stretch (effects rate of contraction)
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8
Q

Normal CO limit (at rest)

A

5 L/min

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9
Q

Maximum CO it can achieve

A

13 L/min

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10
Q

Cardiac output curve demonstrates:

A

The effectiveness of cardiac function at different levels of right atrial pressure (which reflects venous return)

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11
Q

Hyper-effective heart causes (More than normal amount of CO)

A

Sympathetic stimulation

Hypertrophy

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12
Q

Hypo-effective heart causes (less than normal amount of CO)

A

Hypertension
Sympathetic inhibition
Any heart pathology

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13
Q

Factors that decrease peripheral resistance

These can cause:

A

Beriberi (Thiamin deficiency)
Arteriorvenous fistula
Hyperthyroidism
Anemia

Cause pathologically HIGH cardiac output

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14
Q

Abnormal connection between an artery and vein

A

Arteriovenous fistula

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15
Q

Inability to hold O2 in the blood

A

Anemia

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16
Q

Too much fluid in the cardiac sac

A

Cardiac tamponade

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17
Q

Cardiac factors that can cause pathologically low CO

A

Myocardial infarction
Severe valve disease
Myocarditis
Cardiac tamponade

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18
Q

Peripheral factors cause it pathologically low CO

A

Decreased blood volume (hypovolemia)
Acute venous dilation (SNS suppression)
Large vein obstruction
Decreased metabolic rate of tissues (hypothyroidism)

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19
Q

When cardiac output falls too low, it is called:

A

Circulatory shock

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20
Q

Venous return curve plateau is due to

A

Low atrial pressures leading to vein collapse

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21
Q

The higher the right atrial pressure, the _____ venous return will be

A

Less

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22
Q

Venous return curve- mean systemic filling pressure

A

The venous return becomes 0 when the right atrial pressure rises to mean systemic filling pressure

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23
Q

If first atrial pressure is in the negatives, what happens to venous return

A

Increases until it gets to plateau

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24
Q

What happens to CO when sympathetic stimulation increases

A

It increases as right atrial pressure increases

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25
What happens to CO and VR curves during exercise? What happens to right atrial pressure?
Increase Does not really change—- should never really change!!!!
26
If resistance increases, what happens to VR?
It decreases
27
What happens to VR if systemic filling pressure (Psf) increases?
It increases
28
Normal systemic filling pressure
7
29
2 ways to increase delivery (X) of a substance | Fick’s Principle
1- increase it’s concentration [x] 2- increase flow into a tissue (Q)
30
Equation of Fick’s principle
X = Q [x] X = delivery Q = flow into a tissue [x] = concentration Just know what calculation is for, don’t worry about the math
31
What does Fick’s principle calculate?
Cardiac output by solving for Q Q = X/[x] [x] can be measured by [x]art - [x]vein
32
How can you apply Fick’s principle?
By measuring oxygen uptake from the lungs, and blood gas measurements
33
If a tissue is metabolically active, it will have an increase demand for”
Oxygen
34
Most important determinant for how much blood flow is needed in a spot
Local-autoregulation
35
To maintain blood pressure when tissues require a lot of blood, ________ system steps in to help. Why?
Nervous To increase heart rate via sympathetic NS (norepinephrine)
36
Sympathetic (norepinephrine) uses ______ receptors. Which so adrenal (epinephrine) use?
Alpha Beta
37
Mass sympathetic discharge increases:
HR and cardiac contractility
38
In mass sympathetic discharge, what happens to arterioles
They are contracted all over the body except muscles that are working, coronary blood vessels, and cerebral blood vessels
39
During mass sympathetic discharge, what happens to capacitance vessels and reservoirs?
They contract to increase mean systemic filling pressure
40
a result of mass sympathetic discharge
Increase in arterial pressure
41
What can cause increase in anterior pressure? (AKA BP) Which causes higher BP?
Stress Whole body exercises. Stress— there is little muscle activity so there is no vasaodilation, so higher BP
42
Increase arterial pressure increases:
Blood flow directly and indirectly (stress-relaxation of arteries decreases peripheral resistance.)
43
Average blood flow at rest
3-4 ml/min/100g of muscle tissue
44
When skeletal muscle contracts, what happens?
Muscles shorten and widen. They squish the blood vessels. | This causes the blood flow go down
45
Average blood flow during exercise
50-80 ml/min/100g of muscle tissue
46
Left coronary artery and branches supply
The anterior and left lateral portions of the left ventricle
47
Right coronary artery and branches supplies
Most of the right ventricle and posterior part of the left ventricle
48
During systole, coronary blood flow (INCREASES/DECREASES) What about diastole?
Systole decreases Diastole increases
49
Blood vessels on outside of the heart.
Epicardial coronary arteries
50
Cardiac arteries within the heart that cannot be seen on the outside
Subendocardial arteries
51
What arteries in the heart are affected more by the “squish” effect? Impacted more by pressure
Subendocardial arteries
52
Local autoregulation of coronary blood flow is determined by
Local muscle cells’ metabolism; most likely by adenosine secretion in presence of low O2
53
Some epicardial arteries contain ______ receptors. Why?
Alpha 1 vasoconstrictor receptors Thought to help prevent backflow during heavy exercise in the epicardial arteries
54
Coronary mostly contain _________ receptors
Beta2 adrenergic receptors, so general tendency is vasodilation
55
Parasympathetic coronary innervation
Very little direct innervation. Though since Ach slows heart rate, autoregulation leads to decreased blood flow
56
Structure of the blood brain barrier
Continuous capillaries- endothelial cells with tight junctions and lack fenestrae - low amount of vesicular transport Astrocyte foot processes Pericytes
57
Function of the blood brain barrier
Low permeability to most water soluble substances
58
Blood brain barrier needs special carrier systems to transport:
Glucose, amino acids, etc
59
% of the hearts energy is derived from fatty acids at rest
70
60
When must the heart rely more on glucose/glycolysis? What can this cause?
Under anaerobic or ischemic conditions. Results in lactic acid which can cause pain
61
How is adenosine made? What happens with this in the cardiac cell?
ATP degrades to ADP -> AMP -> Adenosine Diffuses out of the cardiac muscle cell and is a potent vasodilator
62
Excessive loss of adenosine can lead to:
Cardiac muscle death
63
About 1/2 of the heart’s adenosine can be lost in”
30 min of ischemia
64
A slow process of plaque formation
Artherosclerosis
65
In artherosclerosis, what happens to cholesterol
Large quantities become deposited beneath the endothelium, scar tissue forms (fibrosis), then calcifies (plaque)
66
Partial or total blockage of coronary arteries leads to:
Ischemia
67
A sudden process with Thrombus and/or embolus
Acute coronary occlusion
68
A penetrating artherosclerotic plaque that can cause a blood clot to form which quickly occluded an artery
Thrombus
69
A thrombus that has broken loose from the site of origin and flows to another site where it lodges
Embolus
70
Congestive heart failure
Failure of the heart to pump enough blood to satisfy the needs of the body
71
Heart failure is characterized by:
A reduced cardiac output and damming up of the venous circulation
72
Heart failure is due to:
Either systolic OR diastolic dysfunction
73
Progressive loss of contractile function of the heart muscle.
Systolic dysfunction
74
Inability of heart to expand enough to fill the ventricles properly
Diastolic dysfunction
75
Which congestive heart failure is more common
Systolic dysfunction
76
Heart failure care also be classified as:
Left sided or right sided
77
Causes of left heart failure: These cause:
Ischemic heart disease Hypertension Valve diseases Myocardial diseases This cause the left ventricle to hypertrophy and/or dilate
78
Left sided CHF leads to:
Pulmonary congestion and edema Decreased renal perfusion leading to water and salt retention
79
Symptoms of CHF
Dyspnea (feeling of not getting enough air) Orthopnea (Breathing effected differently depending on different positions) Cough
80
Causes of right sided heart failure
Left sided heart failure Cor pulmonale (heart problem secondary to a lung problem. So lungs started this, like cystic fibrosis)
81
Pure right sided heart failure leads to
Systemic and portal vein congestion Hepatomegaly and spenomegaly Peripheral edema Kidney congestion leading to water and salt retention
82
What happens to a patient in severe CHF
The pt will manifest with both right and left heart failure symptoms
83
Acutely damaged heart, CO output at 4mmHg right atrial pressure
2ish l/min
84
If the heart is not too damaged from CHF, whaat happens to the excess fluid retention
It actually helps cardiac output by increasing venous return. (Compensated heart failure)
85
What happens w/ excess fluid in a heart severely damaged by CHF
Retention can overwhelm the heart and lead to severe edema and death (decompensated heart failure)
86
Aspects of compensated heart failure
CO will be normal Right atrial pressure is ELEVATED NO further renal salt and water retention occurs Heart MAY recover over weeks and months
87
Aspects of decompensated heart failure
Excessive fluid retention Overstretching of the heart (weakens it further) Pulmonary edema (w/ decreased oxygenation) Renal failure
88
Right atrial pressure at critical cardiac output level for normal fluid balance This indicates decompensated heart disease.
5-11 mm Hg Caused by fluid retention raising the rt atrial pressure over a period of days
89
The kidney needs a min CO of ______ L/min for normal fluid balance
5
90
Renal contribution to progressive decompensated heart failure: Decreased _____ _____ Activation of:
Decreased glomerular filtration Activation of renin angiotensin-aldosterone system
91
What hormone may slow the progression of heart failure
Atrial natriuretic hormone
92
Max percentage that the CO can increase above the normal level
Cardiac reserve
93
Cardiac reserve for normal adult
300-400%
94
Cardiac reserve for athlete
500-600%
95
Cardiac reserve for moderate coronary artery disease
150-200%
96
Cardiac reserve for compensated heart failure
As little as 0%
97
Cardiac reserve for decompensated heart failure
Less than 0%
98
1st heart sound (__) Closure Duration Pitch
``` S1 Closure of AV valves Duration of .14 seconds Lower pitch “Lub” ```
99
2nd heart sound (__) Closure Duration Pitch
S2 Closure of semilunar valves .11 seconds Higher pitch “Dub”
100
3rd heart sounds Happens during: Caused by: Frequency
``` During middle third of diastole Caused by inrushing of blood into ventricles Low frequency (may be audible) ```
101
4th heart sound During: Caused by: frequency:
During atrial systole Caused by inrushing of blood Very low frequency—- very unlikely to hear without any machines
102
Range of sounds that can be heard is between: This is in relation to:
40-520 cycles/second Threshold of audibility
103
Where is auscultation of aortic area checked?
2nd rt intercostal space
104
Where is auscultation of pulmonic area checked?
2nd left intercostal space
105
Where is auscultation of Erb’s point checked?
3rd left intercostal space
106
Where is auscultation of tricuspid area checked?
5th left intercostal space
107
Where is auscultation of mitral area checked?
5th intercostal space at mid-clavicular line
108
Erb’s Point
Spot to hear the best sounds.
109
Aortic Murmur heard during systole
Aortic stenosis
110
Aortic Murmur heard during diastole
Aortic regurgitation
111
Mitral Murmur heard during systole
Mitral regurgitation
112
Mitral murmur heard during diastole
Mitral stenosis
113
Type of murmur that is continuous, although louder during systole
Patent ductus arteriosus
114
Circulatory shock
Generalized inadequacy of blood flow throughout the body to the extent that the body tissues are damaged
115
Cardinal features of circulatory shock inculde:
Decrease in CO | Decrease in BP
116
In circulatory shock, body tissues, including the CV system, begin to:
Deteriorate leading to death within hours or days. it is self perpetuating
117
Causes of circulatory shock via cardiogenic shock
MI Toxicity Valve dysfunction Arrhythmias Something is wrong with the heart
118
Factors that decrease venous return, causing circulatory shock
Diminished blood volume Decreased vascular tone Venous obstruction
119
Stages of circulatory shock
Non-progressive Progressive Irreversible
120
Non-progressive stage of circulatory shock
Compensated stage- where the body’s own compensatory mechanisms will lead to recovery without outside help
121
Progressive stage of circulatory shock
Where shock becomes self-perpetuating until death- is reversible with treatment
122
Irreversible stage of circulatory shock
Severe shock that is refractory to treatment
123
Types of circulatory shock
Hypovolumic / hemorrhagic shock Neurogenic shock Anaphylactic shock Septic shock
124
Shock characterized by decreased systemic filling pressure and therefore decreased venous return. CO and BP then also decrease
Hypovolumic/hemorrhagic shock
125
Hypovolumic/hemorrhagic shock- Non-progressive/compensated stage What happens at 30 sec? 10 min-1hr? 1-48 hours?
30 sec- Baroreceptor reflexes (increase SNS response) Within 10 min to 1 hour- Reverse stress-relaxation response Renin-angiotensin system activation Vasopressin (ADH) Within 1-48 hrs- Absorption of water from interstitial spaces Increased thirst.
126
Progressive stage of hypovolumic/hemorrhagic shock
Hallmarked by progressive deterioration of the CV system (positive feedback loops)
127
Progressive stage of hypovolumic/hemorrhagic shock features:
``` Cardiac depression Vasomotor failure (CNS depression) Blockage of small vessels “slugged blood” Increased capillary permeability (late) Release of toxins Cellular deterioration Acidosis (carbonic and lactic acid) ```
128
Review slide 64
Review slide 64
129
Irreversible stage of hypovolumic/hemorrhagic shock:
Too much tissue damage Too many destructive enzymes and toxins have been released into the tissues Too much acidosis Depletion of high-energy phosphates in the body (creatine phosphate, ATP)
130
Other former of hypovolumic shock other than hemorrhagic
Intestinal obstruction Severe burns Dehydration (sweating, diarrhea, vomiting, nephrotic kidney disease)
131
Neurogenic shock- Hallmarked by: Causes
Hallmarked bu an increased vascular capacity (loss of vasomotor tone) Causes- Deep general anesthesia Spinal anesthesia Brain damage
132
Shock caused by an allergic response to an antigen in the circulation
Anaphylactic shock
133
In anaphylactic shock, basophils and mast cells release: This causes:
Histamine Venous dilation Arteriole dilation Increased capillary permeability
134
Blood poisoning, AKA
Septic shock
135
Septic shock is caused by
A blood borne bacterial infection in which the bacteria has been disseminated throughout the body
136
Damage of septic shock is due to
Infection itself, or due to bacterial endotoxin release
137
Features of septic shock
High fever, Vasodilation Sludging of blood Disseminated intravascular coagulation
138
Treatment of shock
Blood or plasma transfusion Dextran Sympathomimetic drugs Oxygen therapy Glucocorticoids
139
RBC, AKA
Erythrocytes
140
RBC lack:
Nucleus, ER, mitochondria
141
Size of RBS
8 micrometers in diameter | They are biconcave discs
142
Concentration of RBC in the blood
Approx 5 million/cc
143
RBC contains
Hemoglobin (O2 transport. And buffer) And Carbonic anhydrase
144
Process of making blood cells
Hematopoietic
145
Hematopoiesis takes place:
Bone marrow at birth- mostly axial skeleton
146
Hematopoeisis involves what cell types?
PHSC cells (Pluripotent hematopoietic stem cells) CFU-S (Colony-forming unit-spleen)- (Myeloid stem cell) LSC (lymphoid stem cell)
147
CFU-S cells can form
CFU-GM CFU-B/CFU-E CFU-M
148
LSC cells can form
T lymphocytes and | B lymphocyte
149
Genesis of RBC:
Proerythroblast Reticulocyte Erythrocytes
150
For regulation of RBC production, ______ is secreted by __________ in response to low O2 levels in the blood
Erythropoietin (EPO) | Kidneys
151
EPO stimulates:
EBC production in the bone marrow
152
Factors that decrease oxygenation
``` Low blood volume Anemia Low hemoglobin Poor blood glow Pulmonary disease ```
153
Hemoglobin composition
Heme- Iron containing protoporphyrin ring structure Globin- Polypeptide, alpha, beta, gamma or delta
154
Most common types of hemoglobin
HbA - Adult Hg = Alpha2/beta2 HbF- Fetal Hb- Alpha2/Gamma2
155
Iron is absorbed from the:
GI tract
156
Iron binds to ________ to form:
Apotransferrin Forms transferrin which carries the ion in the blood
157
Iron, leased to tissues, will bind to ______ to form:
Apoferritin Forms ferritin which is the storage form of iron in cells
158
What happens when ferritin stores are maximized
An insoluble form of iron storage is hemosiderin
159
Iron excreted from plasma daily
0.6 mg
160
Amount of iron lost daily in menses
0.7 mg Fe
161
Dead hemoglobin enters _______ What happens here? What is excreted?
Macrophages Hemoglobin is degraded, free iron is released Bilirubin is excreted
162
How is iron lost
In feces Bleeding Menstrual loss
163
Avg RBC life span
120 days
164
Why does the metabolism of RBS weaken?
``` So that: Cell membrane becomes less pliable Membrane transport of ions decreases Heme iron goes into the ferric form Oxidation of proteins ```
165
RBCs rupture where?
In the peripheral circulation, or especially in the spleen
166
What phagocytoses damaged RBC?
Kupffer cells
167
Hemoglobin is broken down into ____ and _____ which then break down into _____ and _______
Heme Globin Bilirubin amino acids
168
Deficiency of hemoglobin
Anemia
169
Classification of anemia is based on
RBC size (Normocytic, Macrocytic, microcytic)
170
Anemia classification if based on
Hemoglobin content Normochromic Hypochromic
171
CBC, AKA
Complete blood count
172
What aspects of the CBC indicate anemia?
Low RBC, HCT (hematocrit), and HGB
173
MCV in CBC indicates
Average cell size
174
MCHC and MCH indicates
Hemoglobin content per cell
175
Problem with CBC
It cannot detect abnormalities in shape of cells
176
Types of anemia’s
Hemorrhagic Aplastic Megablastic
177
Cbl, aka cobalamin =
B12
178
Hemorrhagic anemia
Had a bleeding episode, so anemic until you have a transfusion or make new RBC Blood cells lost- normocytic and normochromic
179
Aplastic anemia
Bone marrow not growing RBC- could be genetic, a drug that kills the bone marrow, etc Generally normocytic and normochronic
180
Megaloblastic anemias
Macrocytic, normochromic Anemia of folate deficiency Or Anemia of B12 deficiency Pernicious anemia
181
Anemia B12 deficiency with special mechanism
Pernicious anemia
182
B12 and HC come together to bind,_______ is resp to transport the B12 into the blood
Intrinsic factor (IF)
183
An autoimmune disease keeping us from making intrinsic factor (IF), making it difficult to absorb B12
Pernicious anemia
184
Hemolytic anemia’s
Normocytic, normochromic Shorter lifespan, so lose them faster Hereditary spherocytosis Sickly cell anemia Erythroblastosis fetalis
185
Anemia of iron deficiency
Microcytic, hypochromic
186
Abnormal hemoglobin, causing Hemoglobin S Shapes distorts in absence of O2`
Sickle cell anemia
187
Erythroblastosis fetalis
Mother with Rh- blood type with an Rh+ blood type baby. No problem bc moms blood and babies blood don’t mix. When baby is born and placenta bleeds into the uterine wall. Some of the blood comes in contact with the moms immune system. Causes her to make anti-Rh antibodies. Antibodies can cross the placenta and attack another baby
188
Hereditary sperocytosis
Non spheared blood cells
189
Symptoms of general anemia
Fatigue Weakness Dizziness Paleness of skin
190
High RBC count
Polycythemia
191
What is real active to polycythemia
Intravascular volume depletion | - loss of fluid concentrates blood cells
192
Absolute polycythemia
Actual increase in RBC production
193
Primary polycythemia
Genetic defect involving bone barrow
194
Secondary polycythemia
Consequence of hypoxia, drugs, high altitude, sleep apnea, COPD, etc
195
2 most important blood groups antigens
ABO blood group- possible blood types Rh (rhesus blood group)- gene located on chromosome 1
196
What happens if wrong blood types are mixed
An immune reaction takes place
197
During early childhood, we make antibodies against:
Gut bacteria that have similar antigens to the A and B, unless they are present on your own blood (self vs non-self principle)
198
So, type A RBC have antibodies against
B types
199
People only make anti-rh antibodies if:
They are Rh negative and they are exposed to Rh positive blood in their life.
200
Review slide 94 chart
Review slide 94
201
Most common blood type
O+
202
Rarest blood type
AB-
203
Hemostasis =
Prevention of blood loss
204
Steps of hemostasis
Vascular spasm Platelet plug formation Fibrin clot formation Retraction
205
Vascular spasm
Constriction of blood vessels reducing the rate of blood loss.
206
What can cause vascular spasm?
Pain, vascular wall damage, or thrombocytes A2
207
Platelet plug formation
Activated platelets forming a weak plug
208
Fibrin clot formation (coagulation)
A series of clotting factors are involved in forming a clot
209
Retraction in homeostasis
“Shrinking” of a clot material to approximate edges of would together
210
Platelets are formed where?
In bone marrow from megakaryocytes
211
What do platelets contain?
Actin and myosin
212
What do platelets store?
Calcium
213
Platelets synthesize:
ATP, ADP, prostaglandins, fibrin-stabilizing factor, thrombocytes A2, and growth factors
214
Platelets have _____ ______ that stick to exposed ______
Surface glycoproteins Collagen
215
Lifespan of platelets
12 days
216
Primary hemostasis-
Platelet plug formation
217
What happens when platelets encounter damaged blood vessel wall?
Platelets swell and send out pseudopods that stick to the vessel wall
218
After platelets swell and send out pseudopods that stick to the vessel wall, what happens?
Contractile proteins contract This causes release of factors including ADP and thromboxane A2; these factors activate other platelets, and promote vascular spasm
219
What happens to newly activated platelets
They stick to the growing plug
220
Secondary hemostasis
Coagulation, clot formation Platelet plugs are strengthened by the clotting process
221
Clotting factors for 2ndary hemostasis
``` 1- Fibrinogen 2- prothrombin 3- Tissue factor 4- Calcium 5- label factor 6- obsolete factor 7- stable factor 8- anti-hemophilia factor 9- Christmas factor 10- Stuart-prower factor 11- Plasma thromboplastin 12- Hangeman Factor 12- Fibrin stabilizing factor ```
222
Hemostasis clotting cascade
Intrinsic and extrinsic pathways ——> common pathway
223
Final common pathway for clotting
Prothrombin Activated by prothrombin activator Ends with cross-linked fibrin fibers
224
Extrinsic pathway for clotting
Tissue trauma -> Tissue factor -> prothrombin activator
225
See slide 103
Slide 103
226
Review slide 104
Slide 104
227
Prothrombin time states:
The lower the concentration of clotting factors such as prothrombin, the longer it takes for blood to clot
228
What test is used to help detect and diagnose a bleeding disorder?
Prothrombin Time (PT)
229
Prothrombin time test can also be used to monitor:
How well an anticoagulation medication is working to prevent blood clots
230
Contraction of platelets tighten the clot and pull the edges of the wound together
Clot retraction
231
What are ways to prevent unwanted clotting?
Keeping an intact blood vessel wall Glycocalyx Thrombomodulin
232
What effect does glycocalyx have?
It repels platelets and clotting factors
233
What effect does thrombomodulin have?
Inhibits thrombin | Activated the anticoagulant “protein C” which in turn inactivates factors V and VIII
234
Purpose of anticoagulants
To limit the size of the clot
235
Types of anticoagulants
Heparin | Antithrombin
236
What does heparin bind with
Antithrombin
237
What does antithrombin bind with
Thrombin
238
What is heparin used in surgery for?
To prevent blood clots
239
Lysis of blood clots is done by
Plasminogen activator (tissue plasminogen activator, TPA)
240
Plasminogen activator is released by what?
By damaged tissues over time as they heal
241
Plasminogen activator converts _____ to _____. | When?
Plasminogen Plasmin When the concentration of the activator is great enough
242
What does plasmin digest?
Fibrin clot
243
Plasminogen can be used to:
Digest thrombi (abnormal clots)
244
Bleeding disorders
Vitamin K deficiency Liver damage/disease Hemophilia thrombocytopenia
245
Factors that need vitamin K for their synthesis by the liver
Factors II, VII, IX, and X
246
What is the source of many clotting factors?
The liver
247
What causes hemophilia?
Inheritance of a faulty factor VIII gene. It is an X-Linked trait
248
Lack of platelets (petechial rash = red spots visible on the skin)
Thrombocytopenia
249
Abnormal clots that form on roughened endothelial surfaces (atherosclerosis, infection, trauma)
Thrombi
250
Thrombi that have broken loose from their attachment and may large elsewhere in the circulation
Emboli
251
Unwanted clots may be dissolved clinically how?
By administering plasminogen activator
252
Nerves used for circulation regulation
Sympathetic (norepinephrine) Adrenal (epinephrine)
253
Attempt by the body to restore blood supply to ischemic tissue
Collateral circulation
254
What happens in collateral. Circulation during plaque formation?
Angiogenesis may occur
255
What happens after acute occulsion of the collateral circulation?
Angiogenesis is too slow to restore blood flow acutely, However, vasodilation os collateral vessels may prevent some cardiac muscle death
256
Ischemic heat disease includes:
Angina pectoris Coronary artery disease Myocardial infarction Sudden cardiac death
257
Chest pain
Angina pectoris
258
2 types of angina
Chronic stable angina Unstable angina
259
Angina is often a prelude to _____ if not treated
MI
260
Myocardial infarction results from
An acute coronary occlusion- muscle has little or no blood flow
261
What happens to the affected area of a MI?
It ceases to function and may die
262
MI most commonly affects what part of the heart?
Left ventricle
263
Causes of death due to MI:
Decreased cardiac output Pulmonary edema and kidney failure Fibrillation Cardiac rupture
264
Decreased CO usually occurs when?
When more than 40% of the left ventricle is infarcted
265
Systolic stretch exacerbates the decrease in:
CO
266
How does MI cause pulmonary edema and kidney failure?
Results from the backlog of blood in the body’s venous system
267
Fibrillation may result from:
Leakage of K+ from infarcted area Formation of an “injury current” (ischemic muscle cannot repolarize effectively) Sympathetic reflexes Bulging weak muscle sets up “circus movements”
268
Cardiac rupture happens (OFTEN/RARELY)
Rarely
269
An infarct area of the heart has a central area of: And a peripheral area of:
Dead cardiac myocytes Non-functional but living myocytes
270
Dead fibers from MI are replaced by what?
Scar tissue
271
What happens to nonfunctional fibers after recovery of MI?
They either die, or recover (if reversible) when clot is dissolved, or collateral circulation is adequate
272
What happens to scar tissue on the affected MI area over time?
It retracts (shrinks) Normal tissue hypertrophied over time to compensate for tissue lost
273
Lifestyle treatments for ischemic heart disease
Lose weight Eat a diet low in saturated fat and cholesterol Exercise
274
Other treatments for ischemic heart diseases
Nitroglycerin (vasodilator) Beta blockers TPA (tissue plasminogen activator) Bypass surgery Angioplasty

CVP (4 decks)

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