Physio lecture 1 Flashcards

1
Q

3 principle components of CV system
Func impacted by

A

Heart (pump)
Blood vessels/vascular system (tubes)
Blood (fluid connective tissue)

CV func impacted by endocrine, nervous and urinary systems

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2
Q

Blood formed of

A

cells and cell fragments in liquid called plasma
erythrocytes
leukocytes
platelets

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3
Q

What is hematocrit

A

% of blood volume that is erythrocytes

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4
Q

RBCs func
contain?
shape?

A

Func: gas transport!
contain large amounts of hemoglobin
Biconcave shape -high surface area for improved diffusion

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5
Q

Platelets
contain?
produced when?
role in?

A

-Circulating, colorless, non-nucleated fragments that contain granules-smaller than RBCs
-produced when large bone marrow cells (megakaryocytes) pinch off into circulation
-role in clotting

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6
Q

Blood vessels
arteries and veins do what
exception to rule?

A

Arteries carry blood away from heart (oxygenated)
veins carry to the heart (deoxygen)

except:
Pulmonary arteries- carry deoxy blood to lungs to get oxygen.
Pulmonary veins-carry oxygen blood to heart to get delivered to body

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7
Q

Pressure
what is it
blood flows from..

A

-force exerted by blood -measured in Hg
High pressure area to low pressure area

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8
Q

Flow
what is it

A

-volume of blood moved per unit time (velocity)
ml/min

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9
Q

Resistance
what is it

A

-describes how difficult for blood to flow between two points at any given pressure difference

measure of friction that impedes flow

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10
Q

Resistance
factors that determine it

A

-blood viscosity
-total vessel length
-radius of vessel (radii of vessels is NOT constant- determines changes in resistance)

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11
Q

Epicardium
what kind of tissue

A

fibrous outer layer

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12
Q

Myocardium
composed of?
acts as?

A

middle layer
cardiac muscle
contractile layer

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13
Q

Endocardium
continuous with?

A

inner layer
continuous with lining of blood vessels entering and leaving heart

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14
Q

Atria
L and R what they receive from where

A

R atrium gets deoxy blood from systemic and coronary circulations

L atrium gets oxyg blood from pulmonary circulation

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15
Q

Ventricles
whole shabang

A

R ventricle pumps deoxy blood to lungs

L ventricle pumps oxy blood to rest of body including myocardium

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16
Q

R and L sides of heart- which circuit is which

A

Right-Pulmonary circuit
Left-Systemic circuit

17
Q

Valves

A

2 AV- open in diastole (tricuspid and mitral)

2 semilunar- open in systole (pulmonic and aortic)

S1 (lub)-closure AV valves
s2 (dub)-closure semilunar

18
Q

Coronary arteries
supply
max when

A

-supply oxygenated blood to myocardium
-max in diastole and min in systole

Left CA also has LAD(widowmaker)
Right CA

19
Q

Cardiac veins
do what
coronary sinus

A

-drain deoxy. blood from myocardium
-runs parallel to arteries
-CS- collects blood from veins and returns to R atrium

20
Q

Innervation
Para
Symp

A

Para- vagus nerve -decreases HR and force of contraction
Symp- cardiac splanchnic nerves- increases HR and force of contraction

Visceral afferent pain fibers follow symp pathways to T1-4 (referred chest pain from MI)
Other visceral afferents (stretch, baroreflexes, chemoreflexes) conveyed to brainstem via vagus nerve

21
Q

Cardiac muscles

A

-arranged in tight layers that circle chambers
-every heart cell contracts with every beat of the heart
-LIMITED healing ability

22
Q

Cardiac communication

A

-1% of cells do not contract, instead excite
-Conducting system is in electrical contact with muscle via gap junctions
-this system INITITIATES heartbeat and spreads AP through heart

23
Q

Conducting system sequence

A
  1. SA node-pacemaker, initiates HB, altered by ANS
  2. AV node -receives pulses from SA and passes to bundle of His
  3. Bundle of His- transmits impulses to IV septum-> Purkinje fibers to distribute impulse to ventricular muscle
24
Q

Nodal cells APs

A

SA- NO steady resting potential, undergoes slow depolarization called -Pacemaker potential
—AUTOMATICITY!!!!
Other cells slower, they are driven to threshold by APs from SA
Faster conduction wins!

25
Q

Excitation-contraction coupling

A

-Small amount of Ca enters cell through channels during plateau of AP
-Trigger Ca binds to ryanodine and triggers release of lots of Ca
-This causes a contraction

26
Q

Systole vs diastole

A

Period of ventricular contraction and blood ejection ->Systole

Period of ventricular relaxation and blood filling ->Diastole

27
Q

Periods during systole

A

-Isovolumetric ventricular contraction: ventricles contracting but BLOOD CANNOT leave since VALVES are CLOSED

-ventricular ejection: muscles fibers shorten and blood is forced out. Aortic and pulmonary valves open by RISING PRESSURE
SV is volume of ejected blood from each ventricle during systole

28
Q

Periods during diastole

A

-Isovolumetric ventricular relaxation: valves close and NO BLOOD enters or leaves ventricles

-Ventricular filling: AVs are open, blood flows into ventricles
Atria contract at end but a lot of filling is passive

29
Q

CO formula

A

CO= HR x SV
volume of blood pumped out per unit time
norm: 5 L/min
Resting= SV constant
blood loss=SV declines and CO maintains by increasing HR

30
Q

Regulating HR

A

SA node fires 60-100 x/min

Para(vagus nerve) causes HR decrease
symp causes increase HR

Chronotropic effects

Major factors: increase Epi, increase symp nerves, decrease para nerves-> SA node increased HR

31
Q

SV control

A

-volume of blood each ventricle ejects during contraction
SV= EDV-ESV
70 ml/beat avg.

Regulation:
Preload: changes EDV
afterload: arterial pressures against which ventricles pump

32
Q

Frank Starling

A

Ventricle contracts more forcefully when filled to greater degree during diastole

OPTIMAL LENGTH- increasing EDV leads to this greater stretch and forceful contraction

increase in venous return forces increase CO by increasing EDV and therefore SV

33
Q

Symp Regulation SV

A

NE acts on beta-adrenergic receptors to increase ventricular contractility (Inotropic)

Symp stimulation of myocardium causes powerful contraction but ALSO the contraction and relaxation occurs more quickly

34
Q

Ejection Fraction

A

Quantifies contractility

EF= SV/EDV

avg. 50-75%
increased contractility causes increased EF
this can dx HF

35
Q

Effects of afterload on SV

A

-increased arterial pressure reduces SV
-arterial pressure that constitutes load is termed afterload

greater load= less contracting fibers can shorten at a given contractility