Physiology: Cv

Front 1

the lymphatic system has no

Back 1

pump

Front 2

3 layers of the CV system (vessels)

Back 2

tunica intima (intimate with the blood)
tunica media (muscular)
tunica adventitia (supporting layer)

Front 3

3 layers of the heart

Back 3

endocardium (tunica intima)
myocardium (tunica media)
epicardium (tunica adventitia)

Front 4

parts of the myocardium

Back 4

Purkinge fibers + muscle

Front 5

the myocardium is thickest when

Back 5

the ventricles

Front 6

the vessels feeding the aorta in the adventitia are

Back 6

vasa vasorum

Front 7

3 types of vessels in the arterial system

Back 7

elastic
muscular
arterioles

Front 8

3 layers of the aorta

Back 8

intima
media (predominantly muscle)
adventitia

Front 9

vessels in adventitia of heart:

vessels in adventitia of aorta:

Back 9

coronary arteries
vasa vasorum

Front 10

flattened cells that embrace the capillary endothelial cells
-may have contractile function

found in microcirculation! (capillaries...)

Back 10

pericytes

Front 11

capillaries with large diameters are called

Back 11

sinusoids

Front 12

major pressure drop occurs where?

Back 12

The major pressure drop occurs in the small arteries & arterioles

Front 13

what principle explains:

Blood velocity slows as the cross-sectional area of the vascular bed increases

Back 13

conservation of mass

Front 14

what's the Ca cycle in cardiac muscle contraction?

Back 14

Front 15

what's the Starling law?

Back 15

Front 16

Imagine an experiment in which the aortic valve is kept shut by a very high pressure in the aorta (afterload)

Maximal isometric pressure generated by ventricle during systole ___ as ventricular end-diastolic volume inc

Back 16

inc

Front 17

determinants of the left ventricular systolic curve

the left ventricular diastolic curve?

Back 17

LV systolic: contractility (ex:coronarry artery thrombosis causes an acute reduction in blood flow to the myocardium that may reduce contractility)

LV diastolic: compliance certain conditions may impair diastolic filling of the ventricle...for example, myocardial ischemia impairs diastolic relaxation, while withstanding HTN causes the LV to grow abnormally thick and stiff....

Front 18

determinant of LV diastolic curve

Back 18

compliance

Front 19

determinant of LV systolic curve

Back 19

contractility

what would inc contractility? dec?
inc: epinephrine, digitalis
dec: coronary artery thrombosis

Front 20

Why is it illegal to perform pericardiectomies on greyhounds in the state of FL?

Back 20

the pericardium constrains the LV diastolic curve...without it, SV, CO inc

Front 21

Contraction results in reduction in circumference and decrease in longitudinal axis with ascent/descent of base of heart

Back 21

Front 22

Atrioventricular (AV) valves: tricuspid & mitral valves -Leaflets are attached to _____, which are attached to ____: prevent eversion during ventricular systole


Semilunar valves: aortic & pulmonic valves

Back 22

chordae tendinae

papillary muscles

Front 23

dif bw right side and left side of heart

Back 23

Front 24

The right atrial pressure can be estimated by examining the ______

Back 24

jugular venous pressure

Front 25

pressure-volume loop

Back 25

Front 26

how does inc in contractility affect SV?

Back 26

inc contractility allows ejection to a smaller end-systolic volume...(bc more has pumped out)

Front 27

increased preload's effect on SV?

Back 27

increases SV by ejecting from a greater LVEDV to the same LVESV (not the inc systolic pressure, due to the Frank Starling mechanism)

Front 28

increased afterload's effect on SV?

remember, we just looked at the 3 determinants of SV which are
1) contractility
2) pre-load
and 3) after-load

Back 28

Front 29

how can we measure CO?

Back 29

Front 30

Back 30

a

Front 31

differences in cardiac and skeletal muscle contraction?

Back 31

Front 32

Why do we care about RYR2?

Back 32

heart failure


remember the connection between heart failure and “leaky” RYR2 channels

Front 33

The 5-Phases of the Fast-Response AP

Back 33

Front 34

Slow-Response AP (SA, AV Nodes)“The ionic basis of automaticity”

Back 34

Front 35

Ltcc: L-type calcium channel

When skeletal muscle is stimulated by somatic motor axons, influx of Na+ quickly depolarizes the skeletal myocyte and triggers calcium release from the sarcoplasmic reticulum. In cardiac myocytes, the release of Ca2+ from the sarcoplasmic reticulum is induced by Ca2+ influx into the cell through voltage-gated calcium channels on the sarcolemma. This phenomenon is called_______and increases the myoplasmic free Ca2+ concentration causing muscle contraction. In both muscle types, after a delay, (the absolute refractory period), Potassium channels reopen and the resulting flow of K+ out of the cell causes repolarization to the resting state.

The voltage-gated calcium channels in the cardiac sarcolemma are generally triggered by an influx in sodium during the "0" phase of the action potential

Back 35

calcium-induced calcium release

Front 36

dif bw relative and effective refractory periods

Back 36

Front 37

basal rate of SA node

Back 37

Front 38

ectopic atrial foci

Back 38

Front 39

AV node

Back 39

Front 40

Purkinge fibers

Back 40

Front 41

modulators of pacemaker rate

Back 41

Front 42

Cardiac v. Skeletal Muscle APs
3 KEY differences

Back 42

Plateau Potentials
--Cardiac AP (~ 300 ms)
--Skeletal muscle AP (~ 5 ms)
Long duration prevents the fusion of individual twitches (tetany)

Cell-to-Cell Conduction (via gap junctions)

Automaticity
--Intrinsic pacemakers self-generate APs w/o external triggers

Front 43

current flow through gap junctions

Back 43

Front 44

what's the normal conduction pathway

Back 44

Front 45

Slow/fast APs originate in the SA node.
(automaticity)

slow/Fast APs propagate through atrial muscle via gap junctions.

Slow/fast APs in AV node delay conduction to ventricles

Fast/slow APs rapidly depolarize Purkinje and ventricular muscle

Back 45

Slow APs originate in the SA node.
(automaticity)

Fast APs propagate through atrial muscle via gap junctions.

Slow APs in AV node delay conduction to ventricles
Fast APs rapidly depolarize Purkinje and ventricular muscle

Front 46

re-entrant conduction

Back 46

Front 47

t/f blood flow through only one capillary bed before it goes back to the heart

Back 47

f

Front 48

t/f pulsatile flow is maintained only till the end of the aorta

Back 48

false

Front 49

why don't capillaries rupture?

Back 49

small diameter!

Front 50

Capillary Blood Pressure (PC) Falls from Approximately __ mm Hg at the Arteriolar End to Approximately ___mm Hg at the Venular End

Back 50

35

15

Front 51

lymphatic drainage:

Terminal lymphs return fluids and proteins to circulation via ____
______valves.
Fluid pumped via _____

Back 51

thoracic duct
One-way

skeletal muscle contraction

Front 52

what happens in dehydration, and severe malnutrition in regards to outward pressure and inward pressure

Back 52

Front 53

myogenic response?

Back 53

Front 54

endothelial shear?

Back 54

Front 55

what's the metabolic way of autoregulation?

Back 55

Front 56

what's this?

Back 56

Age-related medial degeneration with elastocalcinosis.

Front 57

arterial pulse pressure correlates with_____

Back 57

stroke volume

Front 58

The equilibrium pressure in the circulatory system when Q = 0 is called the

Back 58

mean systemic pressure, or Pms*

shown is vascular function curve aka venous return curve

Front 59

what's unstressed volume

Back 59

Unstressed volume is the amount of volume needed to “round out” the shape of a vessel before any pressure is generated. Venoconstriction inc the stressed volume.

Front 60

how does blood volume chance Pms?

Back 60

Front 61

Changes in resistance alter the slope of the vascular function curve

Back 61

Front 62

what's venous return

Back 62

Front 63

how do we combine the cardiac function curve and the vascular function curve?

Back 63

Front 64

how does a blood transfusion affect the curves?

Back 64

Front 65

how does reduced contractility affect the curves?

Back 65

Front 66

how different factors affect the cardiac response + venous return curves

Back 66

Front 67

this is what hemorrhage without compensation looks like...what does w/compensation look like?

Back 67

Front 68

Imagine an acute dec in LV contractility, as with ischemia.

what happens to RV and LV CO?

Back 68

Front 69

Young pts with robust compensatory mechanisms can lose a considerable amount of blood before developing hypotension

If you give a drug that reduces _____(for example, morphine) to such a patient, severe hypotension can result.

Back 69

venomotor tone

Front 70

how can LV failure cause pulmonary edema?

Back 70

LV failure can cause pulmonary edema because of elevated pulmonary capillary hydrostatic pressures. Respiratory failure & death can result

Front 71

what's SVR?

Back 71

Front 72

okay, so we know that CO= (Parterial-Pvenous)/SVR

SVR= systemic vascular resistance

but how do we calculate Parterial...if blood is still pulsatile in the arteries!!!

Back 72

mean arterial pressure!

Front 73

what are the factors of vascular resistance?

how does viscosity, radius, and vessel length affect resistance exactly??

Back 73

Front 74

how does viscosity of fluid affect resistance to flow?

Back 74

Front 75

dif bw laminar and turbulent flow?

Back 75

Front 76

compliance?

how do aa and vv compare?

which has greater?

Back 76

Front 77

where in the vasculature does blood have the smallest velocity?

Back 77

capillaries

Front 78

where in the vasculature is:
resistance the highest?
velocity the lowest?
blood volume the lowest? (aa or vv?)
pressure the lowest?

Back 78

resistance the highest? arterioles
velocity the lowest? capillaries
blood volume the lowest? (aa or vv?) aa
pressure the lowest? vv

Front 79

2 types of resistance vessels in the skin

Back 79

Arterioles: found in apical (glabrous) & nonapical (hairy) skin


Arteriovenous anastamoses: found only in apical (highly thermoregulatory) skin

Front 80

Arteriovenous anastamoses & venous plexus

Found in fingertips, palms of hands, toes, soles of feet, ear, nose, lips…)


____ neural control dominates (no metabolic control or autoregulation)

Back 80

Sympathetic

Front 81

symp control of skin?

Back 81

Front 82

t/f
The brain is extremely intolerant of ischemia. Fortunately, it directs its own blood flow.

Back 82

t

Front 83

pH, K+, & adenosine adjust cerebral blood flow to match ______

Back 83

metabolic activity

Front 84

tell me what angiotension II can do...sorta does alot

i know we tend to care that it stimulates the _____ to produce aldosterone but there's other stuff

Back 84

adrenal cortex

Front 85

The heart typically receives ~ 5% of cardiac output
Both LCA & RCA originate at root of ____behind aortic valve cusps

Back 85

aorta

Front 86

LCA supplies LA & LV; divides into

left main artery is the segment between the origin & its bifurcation

Back 86

LAD and LCX;

left anterior descending
and left circumflex

Front 87

______ occurs in 37% of population & can be found arising off LM between LAD and LCX.

Back 87

Ramus intermedius

Front 88

RCA supplies ___, ___, and ____

_____ arises from RCA in ~ 85% of pts; from LCX ~ 15% of pts.

Back 88

RV & RA plus ~ 1/3 of LV (in most pts).

Posterior descending artery

Front 89

what controls myocardial oxygen supply and demand?

Back 89

Front 90

Regulation of coronary blood flow occurs via

Back 90

Physical factors
Neural and neurohormonal factors
Metabolic factors

Front 91

when is coronary artery blood flow the highest? the lowest?

Back 91

Front 92

t/f The subepicardium is more sensitive to ischemia than the subendocardium

Back 92

false

Front 93

effects of symp/para
on
SA node
AV node
myocardium
coronary vessels

Back 93

Front 94

Cardiac sympathetic nerve stimulation leads to:
↑ rate → ↓ time in diastole
↑ contractility → ↑ extravascular compression
Coronary vasoconstriction via alpha receptors

yet, coronary blood flow increases dramatically!

How?

Back 94

Reduction in ATP opens K+ATP channels and causes hyperpolarization, leading to reduced Ca entry and coronary smooth muscle relaxation.

Adenosine stimulates endothelial NO release at low concentrations. At high concentrations, adenosine activates K+ATP channels on vascular smooth muscle.

Front 95

how can reduced coronary artery flow lead to cell death?

Back 95

Front 96

How might the following worsen the balance between myocardial oxygen supply & demand?

Tachycardia (fast heart rate)
Increased contractility
Increased afterload
Increase preload

Back 96

Increase preload

inc force of contraction with resulting inc oxygen consumption

inc chamber size (radius) inc's wall tension

inc intracavitary pressure inc's gradient for subendocardial blood flow

Front 97

how do we measure pulmonary vascular resistance?

Back 97

Front 98

in the lung, where is the blood flow the greatest?

top or bottom?

Back 98

Front 99

zone 1, zone 2, zone 3
which is dead space?

Back 99

Front 100

t/f
inspiration affects alveolar and extra-alveolar vessels differently

Back 100

Front 101

name 2 diseases that can raise pulmonary vascular resistance (PVR)

Back 101