heart as a pump, control of cardiac output - session 2 Flashcards
arteries and veins
- 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
- systemic and pulmonary circulation
- systole and diastole
- 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
pressure in heart, stroke vol.
- stroke vol.
- 70 ml per beat from each ventricle
- 4.9L per min - roughly vol. of blood in body
heart muscle
- discrete cells but interconnected electrically
- cell contraction in response to AP - influx of Ca2+ ions
- cardiac AP relatively long (˜280ms)
heart valves
- opening / closing depends on differential pressure on each side
- cusps of valves attach to papillary muscles vie chordae tendineae
conduction system
- 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
7 phases in cardiac cycle
- 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
abnormal valve function
- stenosis - valve doesn’t opem enough - blood flow obstructed
- regurgitation - valve doesn’t close completely - back leakage when valve should be closed
aortic valve stenosis
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:
aortic valve regurgitation
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
mitral valve stenosis
causes:
- main cause= rheumatic fever (99.9% cases)
- commissural fusion of valve leaflets
- harder for blood to flow LA -> LV
mitral valve regurgitation
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
some key words
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
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
control of cardiac output
afterload, preload, TPR
- 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
pressure
- 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
effects of changing total peripheral resistance (TPR) and keeping Cardiac output (CO) is the same
- TPR falls, CO unchanged -> arterial pressure falls, venous pressure will increase
- TPR increases, CO unchanged -> arterial pressure increased, venous pressure will fall
effects of changing cardiac output (CO) and total peripheral resistance (TPR) is unchanged
- 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
heart must meet changes in demand for blood
- 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
CO, stroke vol. reminder
- 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
ventricular filling
- 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
frank-starling law of the heart
- 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
starling curve
- 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
Length-tension curve for cariac muscle
- if sarcomere length too short filament overlap interferes with contraction
- as muscles are stretched cardiac muscle sensitivity to calcium increases
starlings law
- 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
aortic pressure
- 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)
contractility
- 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
how much the ventricle empties (end systolic volume) depends on
- 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
demand led pumping
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
example - when standing up
- 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
example - during exercise
- 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
summary
- 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
