5. The Heart as a Pump Flashcards
Where does the L ventricle lie?
Under sternum and 4th intercostal space on left
What are the 2 different types of circulations?
Systemic (L.vent -> aorta)
Pulmonary (R.vent -> pulmonary arteries)
NB. same cardiac output in both circulations
Why are the lungs efficiently perfused at a lower pressure than the body?
Pulmonary vascular resistance is much lower than system vascular resistance because the total vascular resistance in the pulmonary vascular bed is much lower than that in systemic circulation.
What is the difference between systemic and pulmonary arteries?
Give their mean pressures.
Systemic: moderate size, thick muscular walls, mean: 100mm/Hg
Pulmonary: large diameter, thin elastic walls, mean: 15mm/Hg
What is Starling’s Law of the Heart?
Ventricular contractile force increases with increased end diastolic volume.
Thus if more blood delivered to R.vent, it expands to greater diameter, and contracts more strongle.
What is preload, and what is it proportional to?
How does an increased preload demonstrate Starling’s Law of the Heart?
What happens to an increased preload in heart failure?
Degree of stretching experienced by the ventricle during diastole. Proportional to end diastolic volume.
An increased preload -> increased end diastolic volume -> increased end-diastolic muscle fibre length -> increased stroke volume and C.O.
Heart failure: ventricles overstretched and weakened, increased preload -> enlarges heart -> weakens it further -> stroke volume decreases
Describe the mechanism underlying Starling’s Law of the Heart
A & M filaments have excess overlap at rest, and stretching INCREASES amount of OVERLAP and thus INCREASES CONTRACTION FORCE.
Thus ventricular contractile force increases in proportion to end disatolic volume.
How is blood prevented from accumulating in the pulmonary or systemic circulation (due to uneven ventricular output)?
Averaged over several beats, the 2 ventricules eject the same volume of blood = balances the output of the 2 sides of the heart
Why is an enlarged heart (detected on an X-ray) a bad sign?
If ventricles enlarged with no corresponding increase in ventricular wall thickness = contracts more weakly than a smaller heart b/c muscle fibres stretched to point where Starling Law does not work anymore, and a LARGE END DIASTOLIC VOLUME produces a SMALLER STROKE VOLUME = heart failure
What is the stroke volume for a normal healthy adult male at rest?
Why is the stroke volume not the same as the end-diastolic volume?
What is the EDV ad ESV in a typical heart?
70ml
Always some blood left in the ventricle at end of systole - residual volume
120ml, 50ml
What is afterload?
How is compliance connected to afterload?
Flow impedence (resistance) of aorta and large arteries. Depends on diameter and elasticity of tissue.
The HIGHER the compliance, the LOWER the afterload, and the LESS WORK the heart has to do
In older people the elasticity of the aorta declines.
a) why is this?
b) what happens to the afterload?
c) how does this affect the stroke volume?
a) elastic tissue progressively lost from the wall and replaced with collagen
b) afterload increases
c) longer period of isovolumetric contraction of the ventricle before aortic valve opens and shorter duration of ejection -> smaller stroke volume -> larger end systolic (residual) volume
an increased afterload decreases C.O.
What is ionotropy?
The contractility of the ventricular muscle. Can vary widely (neuronal and hormonal influence)
How will an increase in contractility affect residual volume and stroke volume?
What factors increase contractility?
Decreases residual volume and thus increase stroke volume
- Increased blood Ca2+
- beta-adrenergic agonists (e.g. adrenaline)
- drugs which stimulate Ca2+ entruy into myocardium (e.g. levosimendan)
- cardiac glycosides (e.g. digoxin)
- insulin & glucagon
Label A-D
A: pulmonary valve
B: aortic valve
C: mitral valve
D: tricuspid valve