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

Question 1

arteries and veins

Answer 1

• 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

Question 2

• systemic and pulmonary circulation
• systole and diastole

Answer 2

• 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

Question 3

pressure in heart, stroke vol.

Answer 3

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

Question 4

heart muscle

Answer 4

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

Question 5

heart valves

Answer 5

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

Question 6

conduction system

Answer 6

• 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

Question 7

7 phases in cardiac cycle

Answer 7

• 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

Question 8

abnormal valve function

Answer 8

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

Question 9

aortic valve stenosis

Answer 9

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:

Question 10

aortic valve regurgitation

Answer 10

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

Question 11

mitral valve stenosis

Answer 11

causes:

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

Question 12

mitral valve regurgitation

Answer 12

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

Question 13

some key words

Answer 13

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

Question 14

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

Question 15

control of cardiac output

afterload, preload, TPR

Answer 15

• 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

Question 16

pressure

Answer 16

• 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

Question 17

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

Answer 17

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

Question 18

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

Answer 18

• 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

Question 19

heart must meet changes in demand for blood

Answer 19

• 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

Question 20

CO, stroke vol. reminder

Answer 20

• 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

Question 21

ventricular filling

Answer 21

• 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

Question 22

frank-starling law of the heart

Answer 22

• 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

Question 23

starling curve

Answer 23

• 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

Question 24

Length-tension curve for cariac muscle

Answer 24

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

Question 25

starlings law

Answer 25

* 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

Question 26

aortic pressure

Answer 26

* 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)

Question 27

contractility

Answer 27

* 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

Question 28

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

Answer 28

* 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

Question 29

demand led pumping

Answer 29

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

Question 30

example - when standing up

Answer 30

* 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

Question 31

example - during exercise

Answer 31

* 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

Question 32

summary

Answer 32

* 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