CV 4 Flashcards

1
Q

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

A

MAP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

MAP = (3)

A

CO x TPR

MAP = (HR x SV) x TPR
MAP = (HR x (EDV-ESV)) x TPR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Flow of blood through the blood vessels

can be thought of as the flow of a

A

fluid

through a tube.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Flow in > Flow out;

A

Hydrostatic pressure in tube will increase due to

fluid accumulation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Flow in < Flow out;

A

Hydrostatic pressure in tube will decrease due to

fluid depletion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

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

A

three

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

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

A

PVP
VR

Systemic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

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

A

Keep MAP constant
Systemic
CO x TPR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Other Baroreceptors

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Patients with chronically elevated MAP have baroreceptor

reflexes that function around a

A

higher than normal setpoint

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Stimuli that decrease MAP (3)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Hypotension

A

Low blood pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Hypotension causes (4)

A
  1. Hemorrhage
  2. Shock
  3. Orthostatic
  4. Other causes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q
  1. Baroreceptor Reflex (2)
A

Returns MAP toward normal

Increasing CO and TPR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q
  1. Autotransfusion (3)
A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q
  1. Endocrine System (2)
A

ANGII, Aldosterone, ADH - Restore volume and osmolarity

Erythropoietin – Restore Hematocrit

25
Q
  1. Behavior (1)
A

Thirst and consumption of H2O

26
Q

Shock

A

This is a condition in which there is inadequate blood flow to meet tissue needs.

27
Q

Three types of shock

A
  1. Hypovolemic shock
  2. Vascular shock
  3. Cardiogenic shock
28
Q
  1. Hypovolemic shock (2)
    results from
    followed by (4)
A

‒ 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
Q
  1. Vascular shock (6)
A

‒ 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
Q
  1. Cardiogenic shock (2)
A

‒ 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
Q

Orthostatic Hypotension

A

Drop in MAP upon standing

32
Q

The effects of gravity cause a

A
decrease VR
decrease EDV
decrease SV
decrease CO
decrease MAP
33
Q

Hypertension

A

Chronically elevated MAP

34
Q

why is hypertension a silent killer?

A

because most people don’t know that they

have it until it has caused significant damage.

35
Q

Prolonged hypertension is the major cause of (4)

A

heart failure,
renal failure,
stroke, and
vascular disease.

36
Q

Two major forms of hypertension

A
  1. Primary (Essential) Hypertension

2. Secondary Hypertension

37
Q
  1. Primary (Essential) Hypertension (2)
A

90% of Hypertension Patients

Idiopathic

38
Q
  1. Secondary Hypertension (3)
A

10 % of Hypertensive Patients
Secondary to a disease state
Treat disease state and MAP returns to normal

39
Q

Factors that are involved in the development of primary hypertension
include: (8)

A
–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
Q

can we cure Primary (Essential) Hypertension?

A

no
We can manage it with diet, exercise, life-style
changes, and medication.

41
Q

Diseases associated with secondary hypertension (6)

A

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
Q

hypertrophic remodeling (5)

A

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
Q

inward eutrophic remodeling (3)

A

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
Q
  1. Laminar Flow

When vessels are: (3)

A

straight
endothelium is healthy
smaller vessels

45
Q

With laminar flow, the velocity of flow is always greater in the

A

center of the vessel compared to the outside.

46
Q

Laminar Flow

— profile of flow

A

Parabolic

47
Q

Shear:

A

When adjacent layers of blood move at different

velocities—can break up RBC aggregates

48
Q

Reynold’s Number (Re) is the calculation of the

A

tendency for turbulent flow

If Re is greater than 2000, flow is most likely turbulent.
Greater than 3000, always turbulent.

49
Q

Re =

A

(V d ρ)/ η

Velocity of blood flow (V)
Diameter of vessel (d)
Density of blood (ρ)
Viscosity of blood (η)—hematocrit

50
Q

Turbulent flow:

increases (3)

A

Increases friction and the energy required to drive flow
Increases the risk of endothelial injury & plaque development
Increases the possibility of thrombotic events

51
Q

Turbulent Blood Flow

in large vessels like (2)

A

Aorta and Pulmonary Artery

52
Q

Smaller vessels

(Arterioles) rarely have

A

turbulent flow

53
Q

Viscosity-

A

thickness or thinness of a fluid

54
Q

Density –

A

measures spaces between 2 particles in a solution

55
Q

Heart Failure (CHF)

A

Heart fails to pump adequate CO

56
Q

Two Types of CHF

A
  1. Diastolic Dysfunction
  2. Systolic Dysfunction

*Many patients have elements of both

57
Q
  1. Diastolic Dysfunction (4)
A

Ventricles have reduced compliance (wall stiffens)
Creates problems with ventricular filling
Reduced EDV
Most common cause = Hypertension (ventricular hypertrophy)

58
Q
  1. Systolic Dysfunction (3)
A

Ventricle has reduced contractility
Decreased SV at any given EDV
Most common cause = myocardial damage as result of
myocardial infarct