Control of Cardiac Output in Systemic Circulation Flashcards Preview

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Flashcards in Control of Cardiac Output in Systemic Circulation Deck (25):

What happens to arterial and venous pressure when total peripheral resistance is decreased with no change to cardiac output?

Arterial decreases
Venous increases


What happens to arterial and venous pressure when total peripheral resistance is increased with no change to cardiac output?

Arterial increases
Venous decreases


What happens to arterial and venous pressure when cardiac output is decreased with no change to total peripheral resistance?

Arterial increases
Venous decreases


What happens to arterial and venous pressure when cardiac output is increased with no change to total peripheral resistance?

Arterial decreases
Venous decreases


Describe demand-led pumping

The heart responds to changes in arterial/venous pressure (key signals) which indicate the body's need for blood.


Describe stroke volume

The difference between end diastolic volume and end systolic volume


How does vein pressure determine the end diastolic volume?

The pressure in the veins determines atrial pressure as there is no valve.
Blood passes from the atria to ventricles, causing the walls to stretch and pressure to rise.
Filling of the ventricles continues until the interventricular pressure is equal to that in the atria.


What is Starlings law of the heart?

Stroke volume is proportional to ventricular pressure, until the pericardium restricts filling.


What does the end systolic volume depend on?

Force of contraction
How hard it is to eject blood


What effect does noradrenaline have on the Starlings curve?

It will steepen the gradient as it improves contractility


Describe what is meant by contractility of the heart

It's intrinsic ability to contract.

Changes in ability to produce force of contraction result from incremental degrees of binding between actin and myosin filaments.


What is ease of ejection of blood from the heart dependent on?

Aortic impedance (sum of external factors that oppose ventricular ejection)
Total peripheral resistance (small effect)


Describe the Bainbridge reflex

High ventricular pressure sensed in the right atrium. Low parasympathetic activity increases heart rate but has no effect on force of contraction.


Describe pressure changes caused by eating a meal and how they are then returned to normal.

Increased activity of gut causes local vasodilation
TPR decreases causing venous pressure to increase and arterial pressure to decrease.
VP increasing causes CO to rise, and AP decreases causes increased heart rate and therefore CO.
Ventricular pressure reduced by extra pumping of the heart which increases atrial pressure.


If the heart rate alone was increased, describe the changes that occur.

CO increase, TPR remains the same
High CO decreases venous pressure and therefore stroke volume. CO returns to original value.


Describe how significant exercises changes pressure and heart rate.

Increase in demand and muscle pumping forces extra blood back to the heart.
Venous pressure will be high and arterial pressure will be low.
The heart rate rises as exercise begins, driven by the brain (CVS centres in medulla). This means that when VP is increased, heart rate is already high which keeps stroke volume down.


Describe how excessive exercise can cause pulmonary oedema

Output of the right and left ventricles can't be matched and there is more entering the right. Causes increased pressure in the lungs, leading to pulmonary oedema


Describe the normal processes that occur when standing up to keep blood pressure constant.

Blood pools in superficial veins in legs due to gravity so venous pressure falls. CO decreases due to Starlings law so arterial pressure also falls.
Baroreceptors sense the low AP, causing heart rate to increase. TPR increases to defend the arterial pressure.
Muscle pumping in the legs increases venous return.


Describe what happens to cause postural hypotension.

When the normal processes used when standing up don't work properly e.g. due to haemorrhage, hypovolaemia, ANS dysfunction causing a transient drop in blood pressure.


Describe the look of a patient with haemorrhage

Pale, high heart rate, sweating, no force to their pulse


Describe the changes to the CVS with a haemorrhage

Low blood volume and venous pressure. CO and arterial pressure also falls.
Volume mostly lost from veins
Increased TPR to increase arterial pressure along with heart rate
Need to increase venous pressure by venoconstriction and autotransfusion.


Describe autotransfusion

Fluid from the ECM is taken up into the CVS to increase circulatory volume


Describe how long term high blood volume can occur

Increased sodium reabsorption in the kidney which causes increased water reabsorption


Describe the effect that long term high blood volume has on the CVS

Increased CO, increasing arterial pressure so VP and AP increased as TPR stays the same.
Overperfusion occurs, autoregulation by metabolite concentration increases TPR so arterial pressure is pushed further up and stayed up.
Average pressure is proportional to volume of the blood.
Causes turbulent flow which can damage the endothelium and increase the risk of atheroma formation


Give some drugs used as treatments for a person with long term high blood volume

Potassium sparing diuretics - amiloride
Thiazide diuretics - chlorothiazide
Loop diuretics