The Heart as a Pump Flashcards
Where and how does systemic circulation occur?
Left heart: contraction of left ventricle pumps blood into aorta
Where and how does pulmonary circulation occur?
Right heart: contraction of right ventricle pumps blood into pulmonary arteries
Why must cardiac output be the same in both systemic and pulmonary circulations?
Otherwise blood will gradually accumulate in one and be removed from the other
How does the left heart function?
Pumps into the aorta and systemic circulation.
The blood pressure in the systemic circulation has to be kept high so that efficient distribution of blood to different organs of the body can occur.
It is like the mains water supply: wherever you turn a tap on in the house, water should come out at a rate determined by the tap opening.
The same is true in the systemic circulation; blood flow to organs is normally determined by the state of constriction of muscles around the small arteries feeding that organ
How does the right heart function? (particularly in terms of pressure)
The right heart pumps into the pulmonary artery and pulmonary circulation.
There is no need for a high pressure here as no distribution of blood to different organs is needed- only the lungs are involved.
The lungs are efficiently perfused at a lower pressure because the pulmonary vascular resistance is much lower than the system vascular resistance.
Pulmonary arterial pressures are lower because the total vascular resistance in the pulmonary vascular bed is much lower than that in the systemic circulation. With a lower vascular resistance a lower pressure is needed from the right heart to push the cardiac output through the pulmonary vessels.
What is Starling’s Law of the Heart and what does it mean?
“Ventricular contractile force increases with increased end diastolic volume”
The fundamental concept here is that when working normally the ventricles will pump out into the aorta whatever volume of blood is delivered to them by the atria.
Thus if more blood is delivered, the ventricle expands to a greater diameter and this makes it contract more strongly.
This concept is incorporated in the idea of cardiac output controlled by preload.
What is preload and what does it determine?
This is the volume of blood delivered to the heart by the superior and inferior vena cava during each diastole.
Thus the preload determines the end diastolic volume (EDV) of the ventricles.
In a normal heart where Starling’s law applies, this in turn determines the stroke volume, i.e. the volume of blood pumped out of the heart per beat.
The stroke volume for a normal healthy adult male at rest is about 70 ml.
The stroke volume is not the same as the end-diastolic volume (ESV), as there is always some blood left in the ventricle at the end of systole.
This blood makes up the residual volume.
In a typical heart, the EDV is about 120 mL and the ESV about 50 mL.
The difference in these two volumes, 70 mL is thus the stroke volume.
How does Starling’s Law relate to preload?
An increase in preload increases end-diastolic volume and thus end-diastolic myocardial muscle fibre length. This stretching increases the force of contraction of the muscle fibres and thus the heart contracts more strongly, expelling the extra volume of blood. The Starling Law is a primitive mechanism that works even in a denervated heart.
Why is an enlarged heart a bad sign?
A heart with enlarged ventricles (where there is no corresponding increase in ventricular wall thickness) will contract more weakly than a smaller heart, as the muscle fibres are stretched to a point where the Starling mechanism no longer works.
A larger end-diastolic volume (EDV) now produces a smaller not a larger stroke volume
When this happens, there is ‘heart failure’
What is the mechanism underlying Starling’s Law?
Cardiac muscle is striated like skeletal muscle.
The contractile mechanism is actin and myosin filaments. One theory is that the filaments have “excess overlap” at low end diastolic volume (EDV); stretching increases the amount of overlap of the active region of the actin and myosin filaments and thus increases the force of contraction
What is afterload?
Afterload is the effective impedance* (dynamic resistance) to flow of the aorta and large arteries. The resistance of the aorta to fluid flow along it depends on the diameter, but it also depends on the elasticity of the tissue. In a dynamic situation like the heartbeat, where the pressure is constantly rising and falling, we should talk about the impedance rather than resistance to flow.
*The reciprocal of impedance is compliance. The higher the compliance of the aorta the lower the afterload, and thus the less work the heart has to do to generate a given cardiac output.
How can you summarise the relation of afterload, preload and contractility to stroke volume?
Increased preload and increased contractility increase stroke volume
Decreased contractility and increased afterload decrease stroke volume
What factors can raise preload? What effect does this have?
Raised due to: - fast filling time - increased venous return Increase end diastolic volume Increase stroke volume
What factors can lower preload? What effect does this have?
Lowered due to: - decreased thyroid hormones -decreased calcium ions - high or low potassium ions - high or low sodium - low body temperature - hypoxia - abnormal pH balance - drugs (i.e. calcium channel blockers) Decreases end diastolic volume Decreases stroke volume
What factors can raise contractility? What effect does this have?
Raised due to: - sympathetic stimulation - epinephrine and norepinephrine - high intracellular calcium ions - high blood calcium level - thyroid hormones - glucagon - beta adrenergic agonists (eg adrenaline) - drugs which stimulate calcium entry into myocardium (eg levosimendan) - cardiac glycosides (eg digoxin) Decreases end systolic volume Increases stroke volume
