Lecture 03 Heart Physiology 2 Flashcards
1. Understand myocardial contractility and how cardiac output is a function of stroke volume and heart rate 2. describe factors affecting stroke volume 3. understand the heart as an endocrine organ 4. describe how treatment is personalised to the patient
How is Cardiac Output measured?
litres per minute
How is Cardiac Output calculated?
heart rate x stroke volume
What is Cardiac Output?
how much blood is being delivered through the circulation per minute
What is the blood volume?
5 litres
this is how much blood is pumped every minute at rest
What is the maximal blood volume with exercise?
35 litres
What is the Ejection Fraction (%)
refers to the percentage volume of blood ejected with each cardiac contraction
normally 55-60% at rest
What factors affect heart rate?
sympathetic stimulation
parasympathetic stimulation
circulating catecholamines
drugs
How does sympathetic regulation affect heart rate?
increases heart rate in response to NA
How does parasympathetic regulation affect heart rate?
decreases heart rate in response to vagus nerve
What is an example of a circulating catecholamine?
adrenaline
When (medically) is sympathetic and parasympathetic regulation irrelevant?
individuals with a heart transplant
no autonomic control
What factors affect stroke volume?
- intrinsic contractility
2. extrinsic contractility
What intrinsic factors affect stroke volume?
intracellular calcium oxygen free fatty acids ATP muscle physiology
What extrinsic factors affect stroke volume?
preload/filling pressure
afterload/resistance to ejection
sympathetic activity
How would you increase a patient’s preload?
injection of saline increases their blood volume and therefore preload
What does intracellular calcium activate? What does this lead to?
ryanodine receptors on the sarcoplasmic reticulum
cascade reaction leading to further activation of ryanodine receptors and release of calcium
How would sympathetic activity affect the stroke volume?
preload and after load kept the same
increasing sympathetic activity increases cardiac output
How does calcium initiate contraction?
calcium attaches to troponin
leads to myosin to be exposed
actin binds to myosin
contraction
How does contraction occur?
- myosin filaments have heads that form cross bridges when attached to actin filaments. ATP is hydrolysed when myosin head is unattached
- ADP+P are bound to myosin as myosin head attaches to actin
- ADP+P release causes head to change position and actin filament to move
- binding ATP causes myosin head to return to resting position
Why is it important that the wave of depolarisation moves through the heart quickly?
so that the whole cardiac muscle can contract together
What does the Frank-Starling Mechanism compare?
cardiac output and end-diastolic pressure
What is end diastolic pressure?
volume of blood in the ventricles at the end of diastole
What is the principle of the Frank-Starling Mechanism?
the bigger the stretch of the myocardial fibres the larger the contraction, this increases the stroke volume and therefore the cardiac output
How does changes in the venous return affect the LVEDP and stroke volume?
increased venous return increases the volume and therefore the LVEDP, this will increase the stroke volume
decreased venous return decreases the volume and therefore the LVEDP, this decreases the stroke volume
Frank Starling Mechanism - what determines how the ventricle operates?
a family of curves determined by afterload and contractility
Frank Starling Mechanism - what happens if the curve shifts up and left?
increased contractility, stroke volume and resistance
decreased afterload
overall increase in cardiac output
Frank Starling Mechanism - what happens if the curve shits down and right?
decreased contractility and stroke volume
increased afterload
overall line is flatter
Frank Starling Mechanism - what effect does the preload have?
curve defined by afterload
move up and down that curve defined by preload
What is Isoprenaline?
synthetic catecholamine similar to NA
What does Isoprenaline do?
enhances calcium influx, increased intracellular calcium causes enhanced contraction
shift Frank Starling curve left and up to a higher cardiac output
Frank Starling Mechanism - what does the curve look like for a failing heart? What does this mean?
curve to the right and down, much flatter
doesn’t matter how much preload is increased, the stroke volume is limited
increasing pressure has little-to-no effect
How is high LVEDP in heart failure patients treated? Why?
diuretics - decrease filling pressure decreases LVEDP
What is a symptom of low cardiac output (medical shock)? What can this lead to if untreated?
breathlessness
heart failure
How is low cardiac output treated?
ACE inhibitors - vasodilation
shift curve left and up increasing CO and decreasing afterload
