Ap1 Cv Systemic Circulation

Front 1

Where is the blood volume distributed in the body?

Back 1

Venous Circulation: 64%
Arterial Circulation: 20%
Pulmonary: 9%
Heart: 7%

Front 2

What is considered the major resistance vessel?

Back 2

Arterioles
(accounts for 50% of resistance)

Front 3

What is the layout of the arterial system?

Back 3

Artery--Arterioles--Metarterioles--Capillaries

Front 4

What are the characteristics of capillary blood flow?

Back 4

Intermittent blood flow
(vasomotion )

Front 5

What is the most important determinant of the degree of opening and closing of metarterioles and precapillary sphincters?

Back 5

Oxygen-- Low O2 increases blood low through capillaries to supply tissue

Front 6

What 3 ways does fluid move across the capillary membranes?

Back 6

1 Diffusion
2 Filtration
3 Pinocytosis

Front 7

Direction of fluid movement with capillary filtration is dependent on four pressures... what are they?

Back 7

1. Capillary pressure
2. Interstitial fluid pressure
3. Plasma colloid oncotic pressure
4. Interstitial fluid oncotic pressure

Front 8

What is the mean capillary pressure ?

Back 8

approx 17 mm/hg
(25mmHg at arterial end, and 10mmHg at venous end)

Front 9

What is the Interstitial fluid pressure and what is it's role in controlling edema?

Back 9

IFP: -6.3mmHg
the negative pressure acts as a vacuum tohold tissues together and maintain a min distance for diffusion of nutrients. Loss of negative pressure allows for edema formation.

Front 10

What makes up the plasma colloid oncotic pressure?

Back 10

Albumin, Globulins and fibrinogen -- total COP is 28mmHg
... causes movement of fluid inward thru cap membranes

Front 11

What is the Donnan Equilibrium effect on COP?

Back 11

extra osmotic pressure attributable to cations (Na+ and K+) attached to dissolved plasma proteins

Front 12

What is the NET effect of the pressure effects of fluid movement across cap membranes?

Back 12

Positive filtration at arterial end and positive reabsorption at venous end...(any extra fluid left in isf is taken up by lymph system)

Front 13

What Lipid soluble molecules DIFFUSE directly through the cap membranes independent of pores?

Back 13

O2, CO2, Inhaled Agents

Insoluable molecules: Na, K, Cl,Glucose(use pores)

Front 14

What molecules are involved in Pinocytosis?

Back 14

High molecular weight molecules: Plasma proteins, Glycoproteins, Polysaccharides

Front 15

How much of the blood volume is in the sytemic circulation?

Back 15

84% (remainder in pulmonary and heart)

Front 16

What is Pulse Pressure?

Back 16

Difference between SBP-DBP

Front 17

What determines PP?

Back 17

Stroke Volume, Heart Rate, Arterial compliance

Front 18

What is the relationship between Pulse Pressure and SV?

Back 18

Increased SV = Increased Pulse Pressure

Front 19

What happens with PP with decreased SVR?

Back 19

Decreased SVR = Increases PP
( flow of blood from arteries to veins is accelerated, which increases venous return and increases SV)

Front 20

What happens with PP with Increased CO?

Back 20

Increased CO = Increased PP

Front 21

What happens to PP with Increased DBP?

Back 21

Inc DBP = Decreased PP

Front 22

What is Pulsus paradoxus? Is this normal or abnormal?

Back 22

An exagerated Decreased in SBP and pulse during Inspiration.(heart cannot expand)
= Patholologic: cardiac tamponade, hypovolemia, restrictive pericarditis.

Front 23

What is Pulsus Alternans? is this normal or abnormal?

Back 23

Alternating weak and strong cardiac contractions... Abnormal:
AV Block
Dig toxicity

Front 24

What is a Pulse deficit?

Back 24

When a second heartbeat is heard thru stehoscope but is not palpable.... Abnormal: AFib or PVC's

Front 25

What is the significance of the phlebostatic angle?

Back 25

Hydrostatic pressure does not alter venour or arterial pressure at this pint. (Tricuspid valve)

Front 26

What happens to Arterial BP if transducer is too high?

Back 26

the reading is low.

Front 27

What determines the viscosity of blood?

Back 27

HCT
also-- increased HCT will decrease PP because of increased resistance.

Front 28

What is the acute controller of Blood flow at the local level?
long term?

Back 28

1. tissue metabolism
2. Oxygen availability
-collateral circulation development

Front 29

What is the Fastest ANS controller of blood flow?

Back 29

1. SNS: NE/E
- Alpha-1 vasoconstriction
- Alpha 2 vasoconstriction
Beta 2 vasodilation

Front 30

What are the Hormonal Vasodilating substances?

Back 30

Bradykinin
serotonin
histamine
Prostaglandins
Low Epi...

Front 31

What are the electrolytes involved in vasodilation?

Back 31

Increased: K+, H+ , CO2, Mg+, Na+

Front 32

What is the Rapid Acting mechanism of Blood pressure?
(sec to min)

Back 32

1.Baroreceptors
-Carotid
-Aortic
2. CNS Ischemic REflex(map<50)
3. Chemoreceptors (dec O2, Inc CO2,H+)
4. Atrial reflexes (bainbridge)

Front 33

What is the intermediate mechanism of blood pressure control?

Back 33

1. Hormonal-(catecholamines, and angeiotension, and ADH vasoconstriction)
2. Intrinsic-capillary shift mechanism
3. Stress-relaxation mechanism

Front 34

What is the long term pressure control mechanism?

Back 34

Renal-body mechanism(Kidneys)

Front 35

What arre the 5 types of shock?

Back 35

Circulatory
Hemorrhagic
Hypovolemic
Neurogenic
Septic

Front 36

What are the characteristic manifestations of shock?

Back 36

1. Decreased CO (except Septic)
2. Reduced Tissue O2 deivery
3. Skeletal muscle weakness
4 Decreased body temp
5. Altered mental status
6. Decreased urine output
7. Progressive deterioration: Cardiogenic Shock