0701- CO as HRxSV and Starlings law- CG

Question 1

Estimate CO and EF (ejection fraction) in a normal person at rest

Answer 1

Cardiac output (L/min) = Stroke volume x HR ie = 0.08L x 70/min

Ejection fraction= SV/EDV ratio (which is the maximal volume in heart at the end of diastolic filling). Usually >55%. (if low may be problem with pump, or hypertension)

Question 2

What are the factors determining CO?

Answer 2

Either affect HR or SV since CO=HRxSV

SV is more complex- affected by preload, afterload, contractility

HR

Electrical- HR (regulated by ANS)

SV

Force of contraction- Preload which sets end diastolic fibre length, contractility, trophic state of cardiac fibre (thick or thin)

Circulatory properties- Afterload (MAP)- ventricular radius (laplace’s law) and systolic BP (and TPR)

Question 3

What is HR regulated by? Why is cardiac output maximal at 130BPM?

Answer 3

By the ANS- Sympathetic increases HR, parasympathetic decreases

SV and HR are inversely proportional (pulse rate↑ = ventricular filling↓)
are roughly equal (what how???) CO= HR^2 (parabolic- maximum value at CO = 130BPM)

…kind of like, CO is the area of a quadrilateral. Given the same perimeter, (sum of SV and HR), what lengths would yield the largest area?

In this case, when HR = 130BPM and SV = ~60mL

Above 130BPM, increased HR insufficent to compensate for loss in SV

Question 4

Know functional properties of cardiac pump: What is preload and how does it determine force of contraction?

What is Frank-Starling law?

Answer 4

Preload = EDV, which sets the ventricular fibre length

(longer fibre length = increased shortening velocity)

Force production = contractility fibre thickness (increased in hypertrophy) x sarcomere length shortening velocity

= ejection↑ → SV↑

In summary Frank-Starling law: ↑preload = ↑SV (within ~2 fold range).

= homeostatic mechanism so that RV = LV output

Question 5

What factors determine preload? Clinical implications

Answer 5

• **compliance: **decreased compliance (stiff ventricle wall) = decreased preload as blood can’t flow in

(compliance = change in volume per pressure during filling)

Decreased compliance seen in fibrosis, myocardial hypertrophy

Increased compliance= dilated cardiomyopathy- (however Laplace’s law- increased afterload due to larger tension force that must be overcome)

• venous return (as outlined in Frank starling law)

Question 6

What are the factors determining contractility?

Answer 6

Isometric force increased if-

high intracellular [Ca2+]

sympathetic activity (B1 receptors) [NB Parasympathetic does NOT affect contractility]

Fibre length (ie preload) and thickness (trophic state of cardiac fibre- see next card)

Exogenous modulators

NA increase via L type Ca, cytosolic ca conc, store refilling via SERCA and troponin 1 (sympathetic outflow signalling cascade)

Hormones- digitalis, B-adrenomimetics, glucagon (↑ contractility), anaesthetics, toxins (decrease)

Diseases- electrolyte, acid base balance, hypoxia, myocarditis,

Question 7

How does muscle tropic state affect contractility?

Answer 7

Force increases with hypertrophy

In athletes- reversible (more contractile proteins produce more force)

However in Hypertrophic CARDIOMYOPATHY - remodelling of fibres (not in parallel)- reduced force production, under B-adrenergic control

Question 8

Define afterload and how it affects SV

Answer 8

= approximately equal to mean arterial pressure (MAP), into which LV need to pump to get blood into aorta.

technically end systolic pressure (at the time when aortic valve closes IT CLOSES IN BETWEEN SYSTOLIC AND DIASTOLIC PRESSURE.

Afterload↑ → SV↓ by decreasing fibre shortening velocity, ejection velocity (ie HTN patients-)

Question 9

What are the determinants of afterload?

Answer 9

Radius of ventricle - Laplace’s Law = tension force proportional to radius

= large ventricle/volume requires more force to contract (ie dilated HF)

**Systemic BP and TPM- **(increase afterload/load into which heart pumps blood into- bad for heart)

**aortic elasticity **(windhessel? reduces afterload?)

Question 10

How does preload affect afterload?

Answer 10

Indirect-afterload↑ → preload↑.

Shortening velocity of fibre↓ → SV↓ → atrial filling pressure↑:

increased afterload (slower shortening velocity) reduces the SV, and increases end systolic volume. remaining ESV gets added onto the next cycle’s preload,

This may take some time

Question 11

Summary

Answer 11

• SV decreases linearly with HR.
• CO is determined by SV and HR.
– HR can be modulated by sympathetic and parasympathetic influences.

– SV can be increased by
• preload ↑ (end-diastolic filling pressure),
• contractility ↑ (sympathomimetics, digitalis, etc.),
• fibre thickness ↑, and
• afterload ↓ (systemic BP, TPR).
• A large ventricle requires more tension force (sarcomere length)
• Ultimately, afterload↑ causes preload↑