CV 4 Flashcards

1
Q

— is the driving force for blood flow to all organs.

A

MAP

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2
Q

MAP = (3)

A

CO x TPR

MAP = (HR x SV) x TPR
MAP = (HR x (EDV-ESV)) x TPR
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3
Q

Factors that influence MAP (3)

A
  1. Flow In (CO) and Out (TPR) of Systemic Arteries
  2. MAP α Total Blood Volume
  3. Distribution of blood between arteries and veins
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4
Q

Flow of blood through the blood vessels

can be thought of as the flow of a

A

fluid

through a tube.

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5
Q

Flow in > Flow out;

A

Hydrostatic pressure in tube will increase due to

fluid accumulation.

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6
Q

Flow in < Flow out;

A

Hydrostatic pressure in tube will decrease due to

fluid depletion.

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7
Q

Systemic Circulation function can be thought of as the function
of — different tubes connected in series

A

three

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8
Q

Venous System
Function: (2)
Regulation: (1)

A

PVP
VR

Systemic

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9
Q

Arterial System
Function: (1)
Regulation: (1)
MAP =

A

Keep MAP constant
Systemic
CO x TPR

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10
Q
Capillary System
Function: (2)
Control: (1)
Ftissue = 
Due to myogenic autoregulation, changes in the Rtissue used to regulate (2)
A

Deliver O2 and nutrients, Pick up CO2 and other metabolic waste
Local (Active Hyperemia)
MAP/Rtissue arteriole
Pc and flow

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11
Q

Baroreceptor Reflex (4)

A
Short term response 
(minutes to hours) 
NS mediated 
homeostatic process
Alters CO and TPR to 
restore MAP to 
homeostatic levels
Override Local Control of 
blood flow
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12
Q
Baroreceptor Reflex
Stimulus = 
Reflex Receptor =
Afferent Pathway = 
Integrating Center = 
Efferent Pathway = 
Effectors =  
Effector Response =  
Feedback Regulation =
A

Stimulus = ΔMAP
Reflex Receptor = Baroreceptors (Aortic Arch and Carotid Arteries)
Afferent Pathway = Visceral Sensory Neurons
Integrating Center = Medullary CV control centers in Medulla Oblongata (Brainstem)
Efferent Pathway = Autonomic Motor Neurons
Effectors = Cardiac Muscle (AR and Contractile cells), Arteriolar Smooth Muscle, Venous Smooth Muscle
Effector Response = Change rate and force of contraction (CO), Change arteriolar resistance (TPR), Change venous tone (VR>EDV >CO)
Feedback Regulation = Negative

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13
Q

Other Baroreceptors

A

Large systemic veins, the pulmonary vessels, and the walls of
the heart also contain baroreceptors.

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14
Q

Baroreceptor Function (3)

A

Immediate changes to restore MAP to homeostatic level
Allows time for other mechanisms to occur to eliminate
disturbance (ex. Total Blood Volume)
Adapt overtime (decrease rate of firing with prolonged increased MAP)

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15
Q

Patients with chronically elevated MAP have baroreceptor

reflexes that function around a

A

higher than normal setpoint

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16
Q

MAP affected by other stimuli and reflexes aside from baroreceptor reflex.
Changes triggered by signals from

A

other receptors or higher brain centers that activate Medullary CV control center or autonomic neurons directly

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17
Q

Stimuli that increase MAP (8)

A
 decrease Arterial [O2]
 increase Arterial [CO2]
 decrease Brain Blood Flow
Pain Originating in skin
Stress
Anger
Eating
Sexual Activity
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18
Q

Stimuli that decrease MAP (3)

A

Pain Originating in Viscera or joints
Sleep
Happy Mood

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19
Q

Hypotension

A

Low blood pressure

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20
Q

Hypotension causes (4)

A
  1. Hemorrhage
  2. Shock
  3. Orthostatic
  4. Other causes
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21
Q
Hemorrhage Compensatory Mechanisms
Rapid (12-24 hours) (2)
Long Term (days to Weeks) (2)
A
  1. Baroreceptor Reflex
  2. Autotransfusion
  3. Endocrine System
  4. Behavior
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22
Q
  1. Baroreceptor Reflex (2)
A

Returns MAP toward normal

Increasing CO and TPR

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23
Q
  1. Autotransfusion (3)
A

Movement of interstitial fluid into capillaries
Arteriolar constriction > decreases PC
Net absorption of fluid into capillaries

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24
Q
  1. Endocrine System (2)
A

ANGII, Aldosterone, ADH - Restore volume and osmolarity

Erythropoietin – Restore Hematocrit

25
4. Behavior (1)
Thirst and consumption of H2O
26
Shock
This is a condition in which there is inadequate blood flow to meet tissue needs.
27
Three types of shock
1. Hypovolemic shock 2. Vascular shock 3. Cardiogenic shock
28
1. Hypovolemic shock (2) results from followed by (4)
‒ It results from a large loss of blood, so there is a drop in blood volume. ‒ This usually follows hemorrhage, severe vomiting, severe diarrhea, and extensive burns.
29
2. Vascular shock (6)
‒ Blood volume is normal, but circulation is poor due to abnormal expansion of the vascular bed caused by extreme vasodilation. ‒ Huge drop in TPR leads to a drop in MAP ‒ The most common causes: • loss of vasomotor tone associated with anaphylaxis (allergic reaction; anaphylactic shock) • a loss of nervous system regulation (neurogenic shock) • septicemia (septic shock; a bacterial infection).
30
3. Cardiogenic shock (2)
‒ This is pump failure. The heart can not sustain adequate circulation. ‒ This is usually the result of myocardial damage following a severe MI or multiple MIs.
31
Orthostatic Hypotension
Drop in MAP upon standing
32
The effects of gravity cause a
``` decrease VR decrease EDV decrease SV decrease CO decrease MAP ```
33
Hypertension
Chronically elevated MAP
34
why is hypertension a silent killer?
because most people don’t know that they | have it until it has caused significant damage.
35
Prolonged hypertension is the major cause of (4)
heart failure, renal failure, stroke, and vascular disease.
36
Two major forms of hypertension
1. Primary (Essential) Hypertension | 2. Secondary Hypertension
37
1. Primary (Essential) Hypertension (2)
90% of Hypertension Patients | Idiopathic
38
2. Secondary Hypertension (3)
10 % of Hypertensive Patients Secondary to a disease state Treat disease state and MAP returns to normal
39
Factors that are involved in the development of primary hypertension include: (8)
``` –Diet: high Na+, high cholesterol etc. –Diabetes mellitus –Obesity –Age (clinical signs appear ~40) –Gender (males get it more than females until menopause) –Genetics (runs in families, black more prevalent [salt sensitive forms] than whites) –Stress –Smoking ```
40
can we cure Primary (Essential) Hypertension?
no We can manage it with diet, exercise, life-style changes, and medication.
41
Diseases associated with secondary hypertension (6)
Tumor of the adrenal medulla (excess Epinephrine) Cushing’s disease (Glucocorticoid excess) Atherosclerosis of the renal arteries (RAS) Renal Hypertension (Kidney disease) (RAS) Arteriosclerosis Hyperthyroidism (TH excess)
42
hypertrophic remodeling (5)
Large vessels that do not constrict in response to increased MAP Size of VSM cells increase Increase in EC matrix proteins to support wall increase total cross sectional area of vessel Makes large vessels stiffer (less compliant)
43
inward eutrophic remodeling (3)
Small vessels that constrict in response to increased Map VSM growth around narrowed lumen (decrease r; increase R) No change in total cross sectional area of vessel
44
1. Laminar Flow | When vessels are: (3)
straight endothelium is healthy smaller vessels
45
With laminar flow, the velocity of flow is always greater in the
center of the vessel compared to the outside.
46
Laminar Flow | --- profile of flow
Parabolic
47
Shear:
When adjacent layers of blood move at different | velocities—can break up RBC aggregates
48
Reynold’s Number (Re) is the calculation of the
tendency for turbulent flow If Re is greater than 2000, flow is most likely turbulent. Greater than 3000, always turbulent.
49
Re =
(V d ρ)/ η Velocity of blood flow (V) Diameter of vessel (d) Density of blood (ρ) Viscosity of blood (η)—hematocrit
50
Turbulent flow: | increases (3)
Increases friction and the energy required to drive flow Increases the risk of endothelial injury & plaque development Increases the possibility of thrombotic events
51
Turbulent Blood Flow | in large vessels like (2)
Aorta and Pulmonary Artery
52
Smaller vessels | (Arterioles) rarely have
turbulent flow
53
Viscosity-
thickness or thinness of a fluid
54
Density –
measures spaces between 2 particles in a solution
55
Heart Failure (CHF)
Heart fails to pump adequate CO
56
Two Types of CHF
1. Diastolic Dysfunction 2. Systolic Dysfunction *Many patients have elements of both
57
1. Diastolic Dysfunction (4)
Ventricles have reduced compliance (wall stiffens) Creates problems with ventricular filling Reduced EDV Most common cause = Hypertension (ventricular hypertrophy)
58
2. Systolic Dysfunction (3)
Ventricle has reduced contractility Decreased SV at any given EDV Most common cause = myocardial damage as result of myocardial infarct