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CVS > heart as a pump, control of cardiac output - session 2 > Flashcards

heart as a pump, control of cardiac output - session 2 Flashcards

1
Q

arteries and veins

A
  • arteries = Resistance vessels - restrict blood flow to supply areas in the body where it’s needed
  • veins = Capacitance vessels - enable system to vary amount of blood pumped around the body
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2
Q
  • systemic and pulmonary circulation
  • systole and diastole
A
  • systemic circulation = high pressure
  • pulmonary circulation = low pressure
  • systole = contraction and ejecton of blood from venricles
  • diastole = relaxation and filling of ventricles
  • atria act as priming pumps for ventricles
  • output of left and right sides over time must be equal
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3
Q

pressure in heart, stroke vol.

A
  • stroke vol.
    • 70 ml per beat from each ventricle
    • 4.9L per min - roughly vol. of blood in body
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4
Q

heart muscle

A
  • discrete cells but interconnected electrically
  • cell contraction in response to AP - influx of Ca2+ ions
  • cardiac AP relatively long (˜280ms)
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5
Q

heart valves

A
  • opening / closing depends on differential pressure on each side
  • cusps of valves attach to papillary muscles vie chordae tendineae
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6
Q

conduction system

A
  • SAN - pacemaker - generates action potential
  • activity spreads over atria - causes atrial systole
  • delayed at AVN for approx. 120ms
  • after delay spreads through ventricular myocardium from endocardial to epicardial surface
  • ventricles contract from apex in twisting fashion - blood forced through outflow valves
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7
Q

7 phases in cardiac cycle

A
  • stages 2 to 4 = systole (~0.35s)
  • stages 5 to 1 =diastole (~0.55s)
  • if heart rate increased - diastolic period decreased systolic remains the same
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8
Q

abnormal valve function

A
  • stenosis - valve doesn’t opem enough - blood flow obstructed
  • regurgitation - valve doesn’t close completely - back leakage when valve should be closed
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9
Q

aortic valve stenosis

A

normally opens to around 3-4cm, when stenosed >1

causes:

  • degenerative - senile calcification/ fibrosis
  • congenital - valve is bicuspid instead of tricuspid
  • chronic rheumatic fever - inflammation - commissural fusion

consequences:

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10
Q

aortic valve regurgitation

A

causes:

  • aortic root dilation (leaflets pulled apart)
  • vlavular damage (endocarditis rheumatic fever)
  • blod flows back into LV during diastole - increases stroke vol. - systolic pressure increases
  • diastolic pressuredecreases
  • bounding pulse (head throbbing, quinke’s sign)
  • LV hypertrophy
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11
Q

mitral valve stenosis

A

causes:

  • main cause= rheumatic fever (99.9% cases)
  • commissural fusion of valve leaflets
  • harder for blood to flow LA -> LV
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12
Q

mitral valve regurgitation

A

chordae tendineae + papillary muscles normally prevent prolapse in systole - myxomatous degeneration can weaken tissue leading to prolapse

other causes:

  • damage to papillary muscle after heart attack
  • left sided heart failure leads to LV dilation - can stretch valve
  • rheumatic fever can lead to leaflet fibrosis which disrupts seal formation
  • blood leaking back to LA increases preload as more blood enters in LV n subsequent cycles - can cause LV hypertrophy
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13
Q

some key words

A

myxomatous degeneration - refers to pathological weakening of connective tissue

syncpe= temporary loss of consciousness caused by fall in bp

microangiopathic haemolytic anaemmia = estruction of RBCs as they pass under high pressure through a stenosed valve

rheumatic fever = inflammatory disease

fibrosis = thikening and scarring of connective tissue

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14
Q

Typically a Wigger’s diagram is plotted for just the LEFT side of heart. A diagram for the RIGHT side would be very similar but at lower pressures.

for rest of notes, see dropbox notes/ lecture slides

A
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15
Q

control of cardiac output

afterload, preload, TPR

A
  • afterload -the load the heart must eject blood against - roughly equivalent to aortic pressure (aortic impedance)
  • preload- amount ventricles stretched in diastole - related to end diastolic volume (EDV) or central venous pressure
  • total peripheral resistance - sometimes reffered to as systemic vascular resistance - resistance to blood flow offered by all systemic vasculature
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16
Q

pressure

A
  • pressure exerted by blood drops as it flows through a ‘resistance’
  • arterioles offer greatest resistance
  • constriction of arterioles increases resistance causes…
    • pressure in capillaries on arterial side to rise
    • pressure in capillaries on venous side to fall
17
Q

effects of changing total peripheral resistance (TPR) and keeping Cardiac output (CO) is the same

A
  • TPR falls, CO unchanged -> arterial pressure falls, venous pressure will increase
  • TPR increases, CO unchanged -> arterial pressure increased, venous pressure will fall
18
Q

effects of changing cardiac output (CO) and total peripheral resistance (TPR) is unchanged

A
  • if CO increases, TPR unchanged -> arterial pressure will increase,venous pressure will fall
  • if CO decreases, TPR unchanged -> arterial pressure will fall, venous pressure will rise
19
Q

heart must meet changes in demand for blood

A
  • if more blood needed - arterioles + precapillary sphincters dilater -> TPR falls
  • heart needs to pump more so arterial pressure doesn’t fall and venous pressure doesn’t rise
  • heart ‘sees’ changes in demand as changes in arterial blood presure (aBP) and central venous pressure (CVP)
  • heart respons to changes in CVP + aBP by intrinsic and extrinsic mechanisms
20
Q

CO, stroke vol. reminder

A
  • CO=stroke vol. x heart rate
  • stroke vol. (SV) = end diastolic volume (EDV) - end systolic volume (ESV) - these values can chage to increase SV
  • average SV= 70ml = 67% of normal EDV
21
Q

ventricular filling

A
  • ventricles isolated from arteries during diastole
  • ventricles fill until walls stretch enough to produce an intraventricular pressure equal to the venous pressure
  • the higher the venouspressure the more the heart fills
  • relationship is the ventricular compliance curve - compliance can be increased/ decreased in disease states
22
Q

frank-starling law of the heart

A
  • like skeletal muscle, if fibres of heart stretched before contracting - it will contract harder
  • more the heart the harder it contracts (up to a limit)
  • harder heart contracts - larger the stroke vol.
  • increased venous pressure -> heart fills more
  • how much the ventricles fill depends on compliance
23
Q

starling curve

A
  • increased venous return -> increased let ventricular end diastolic pressure (LVEDP) and volume (increased ‘preload’)
  • increased stroke volume -> more blood pumped out of LV

Normal operating point at rest is when LVEDP around 8mm Hg and stroke volume around 70ml

24
Q

Length-tension curve for cariac muscle

A
  • if sarcomere length too short filament overlap interferes with contraction
  • as muscles are stretched cardiac muscle sensitivity to calcium increases
25
Q

starlings law

A
  • ensures sustemic and pulmonary circulation are balanced by ensuring both sides of the pump maintain the same output
  • same vol. of blood pumped to body must be also pumped to lungs
  • Increased stroke volume with increased filling of the heart is an INTRINSIC control mechanism
26
Q

aortic pressure

A
  • arterial (aortic) pressue is increased when peripheral resistance increased - harder for heart to pump out
  • increased TPR reduces venous pressure - therefore reduces filling of heart
  • overtime can get an inappropriate increase in arterial pressure - heart will have ti work harder (hypertension)
27
Q

contractility

A
  • the force of contraction for a given fibre length
  • increased contractility -> increased force of contraction for a given left EDP
  • extrinsic factors affecting contractility:
    • increased sympathetic stimulation -> increased contractility
    • circulating adrenaline -> increased cotractility
28
Q

how much the ventricle empties (end systolic volume) depends on

A
  • how hard it contracts
    • determined by rnd diastolic vol. (how much it fills) and contractility (increased by sympathetic drive)
    • how hard it is to eject blood, determined by aortic impedance

autonomic NS controls contractility + heart rate

decrease in arterial BP reduces parasympathetic NS activity + stimulates sympathetic NS to increase heart rate + contractility

29
Q

demand led pumping

A

metabolism of body increases - TPR falls - reduced arterial pressure - increased venous pressure - hearts response is to pump more

example - when eating - local vasodilation of gut -see pic

30
Q

example - when standing up

A
  • blood pools in legs due to gravity + both venous + arterial pressures are in the same direction
  • intrinsic mechanisms can’t correct this
  • barroreceptor reflex + ANS increase heart rate + increase TPR- postural hypertension if reflexes don’t work
31
Q

example - during exercise

A
  • muscle pumping and venoconstriction increasesvenous return
    • later decreased TPR also increases venous return
  • very early response= increased heart rate (decrease parasympathetic drive, increased sympathetic drive)
  • increased contractility due to increased sympathetic drive

N.B. increased venous pressure on its own would move ventricular function to the flat part of the Starling curve

32
Q

summary

A
  • Intrinsic control mechanisms ensure that the output ofthe left and right ventricles match
    • frank starling law of heart
  • The heart responds to changes in demand by bothintrinsic and extrinsic mechanisms
    • Starling’s law control and the autonomic nervous system

CVS (5 decks)

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