Download Cardiac Output

Cardiac Output
“volume of blood ejected by each ventricle
each minute”
Pulmonary & Systemic circuits receive similar volumes
Right vs Left output may vary from beat to beat, but
Over short periods “ventricular balance”
balance” is maintained
Venous Return
“volume of blood flowing from the veins
into the right atrium each minute”
NB: must be equivalent to Cardiac Output
Cardiac Output
Key factors that influence CO:
Metabolism
CO varies directly with activity level throughout life
Rest: 4.9-5.6 l/min (young, healthy, female-male)
Exercise: 4-5 fold increase (20-25 l/min)
Age
Metabolic activity declines with increasing age
Body size (Body Surface Area – BSA)
CO increases approximately in proportion to BSA
Gives rise to the Cardiac Index
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Cardiac Index
“cardiac output per square metre of BSA”
BSA (m2 ) = 0.007184 ! Height (cm)0.725 ! Weight (kg)0.425
Jones et al. (1985) A revision of body surface area estimations. European Journal of Applied Physiology (53): 376-379.

BSA ranges from: 1.5-2.5 m2
Guyton & Hall 11th Ed,
Ed, fig’
fig’s 20-1 & 20-2
Cardiac Output
Controlled by two components:
Heart Rate (HR):
number of times the heart beats per minute
Stroke Volume (SV):
volume of blood ejected by each ventricle per heart beat
Cardiac Output (CO) = Heart Rate " Stroke Volume
CO = HR " SV
= 70 beats/min " 70 ml/beat
= 4900 ml/min ! 5 litres/min
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Control of Heart Rate
SA node
Intrinsic firing rate (i.e. without any neuro-humoral input)
= 100 beats/min
At rest (↑
(↑ vagal activity inhibits SA node)
Average HR = 70 beats/min
Achieved via:
Parasympathetic (vagus) cholinergic input ↑K+ permeability
→ hyperpolarisation and slowed drift to threshold
Initial increases in HR to 100-110 beats/min
Achieved via inhibition of parasympathetic tone
(vagal withdrawal)
Control of Heart Rate
Exercise (HR > 110 beats/min)
Achieved via sympathetic stimulation of:
SA node → ↓K+ permeability
→ depolarising effect and faster drift to threshold
AV node → reduced AV node delay via ↑Ca2+ flux
Conduction pathways (Bundle of His, Purkinje cells)
Age predicted Max. HR = 220 - Age
HR Reserve = Max HR - Rest HR
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Sherwood 6th Ed,
Ed, fig 9-20
Control of Stroke Volume
At rest
SV = 70ml (EDV = 140ml; ESV = 70ml)
2 main factors influence SV
Preload (intrinsic mechanism)
Increased filling pressure/volume → ↑EDV
→ cardiac stretch and increased contractility
Contractility (extrinsic mechanism)
Inotropic factors including sympathetic stimulation
→ ↑[Ca2+]i and contractility
3rd factor
Afterload (extrinsic mechanism)
Pressure against which the left ventricle works
Primarily aortic pressure which provides resistance to outflow
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Preload:
Frank Starling law of the heart
Sherwood 6th Ed,
Ed, fig 9-22
Preload: Left & Right Heart
Cardiac Function Curves
Stroke volume
Similar for Left & Right
Despite different filling pressures (i.e.
Atrial Pressures)
Right heart
Marginally greater sensitivity to filling
pressure
Filling pressure
Higher for left heart
Reflects thicker left ventricle
(i.e. greater resistance to stretch
during filling from Left Atrium)
Reflects diastolic filling of Right
Ventricle with little addition from
Right Atrium
Noble & Co.,
Co., fig 4.3
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Preload Summary
Noble & Co.,
Co., fig 4.4
Contractility
Sympathetic nervous input to ventricular muscle
Acts via β1 adrenoceptors
→ G-protein coupled increase in cAMP
→ activation of protein kinase A (PKA)
→ activation of surface L-type Ca2+ channels
Increases [Ca2+]i and Enhances CICR
→ greater contractile force of ventricular myocytes
Increased SV
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Contractility
Sherwood 6th Ed,
Ed, fig 9-24
Summary:
Control of Cardiac Output
Sherwood 6th Ed,
Ed, fig 9-25
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