Control of Cardiac Output Flashcards
Define stroke volume
How is it calculated?
The volume of blood ejected from each ventricle during each ventricular contraction
SV = EDV - ESV
EDV= end diastolic volume
ESV= end systolic volume
Define cardiac output
How is it calculated?
The volume of blood pumped out of each ventricle per minute
CO = HR x SV
Units are L/min
Define ejection fraction
How is it calculated?
Fraction of the end diastolic volume that is pumped out during ventricular systole
EF = SV / EDV x 100
What affects left ventricular stroke volume?
Preload (amount of volume that enters the ventricle before each contraction- end diastolic volume):
- Preload 1: systemic venous return
- Preload 2: right heart function
- Preload 3: pulmonary vascular resistance
- Preload 4: mitral valve (stenosis=reduced preload)
Left ventricular contractility
Afterload (pressure against which the ventricle is ejecting blood):
- Afterload 1: aortic valve diameter
- Afterload 2: arterial blood pressure
- Afterload 3: arteriolar tone (r4)
What factors affect cardiac output?
Heart rate
- ANS
- Atrial reflex (influenced by venous return)
- Hormones
Stroke volume
- End diastolic volume; influenced by:
- Preload
- Filling time (HR)
- Venous return (into R and L atria)
- Preload
- End systolic volume; influenced by:
- Preload
- Contractility
- Hormones
- ANS
- Afterload
- Vasodilation/constriction
How does the preload increase contractility?
Starling’s Law: the more a muscle is stretched, the harder it will contract.
When is ventricular filling most rapid?
How is this affected by increased HR?
How does this affect cardiac output?
How does mitral valve stenosis affect this?
The first half of ventricular filling (the rapid filling phase) is faster as the ventricle is more compliant.
Raised HR will reduce ventricular filling time having most impact on early diastole- the ventricle will have less time to refill and cardiac output will drop.
- Mitral valve stenosis will worsen this as it provides obstruction to blood returning to the left atrium & ventricle from the lungs.
- Atrial fibrillation also worsens this as it reduces atrial systole (further reducing ventricular filling)
How does atrial fibrillation affect ventricular filling?
Atrial fibrillation causes a loss of atrial contraction which is required to overcome the resistance to filling by the ventricles towards the end of ventricular diastole (during diastasis) when the ventricles are less compliant and passive filling slows.
Loss of atrial contraction reduces ventricular filling therefore reduces preload (cardiac output falls)
How does the autonomic nervous system impact HR?
Parasympathetic stimulation (via vagus nerve):
- Slows depolarisation of cardiac muscle (hyperpolarisation)
- Cells take longer to reach the threshold for action potential firing.
Sympathetic stimulation:
- Speeds up depolarisation so the cardiac muscle cells reach threshold for action potential firing much faster.
- Also reduces repolarisation
Describe the baroreceptor reflex
- Baroreceptors in the aortic arch and carotic sinus detect stretch caused by increased blood pressure.
- Increase afferent firing via vagus nerve and glossopharyngeal nerve to cardiac vasomotor centres in the medulla.
- Efferents:
- Increase parasympathetic stimulation via vagus nerve to heart (SA and AV node- increase delay of conduction)
- Decrease sympathetic stimulation of heart.
- Decrease sympathetic stimulation of blood vessels (reducing vasoconstriction).
- Increases nervous input to adrenal medulla to increase noradrenaline release and RAAS system.
- Blood pressure falls
Describe the chemoreceptor reflex
- Increased pCO2 and/or decreased pO2 detected by chemoreceptors in the carotid body and aortic arch.
- Increased firing of chemoreceptors via vagus and glossopharyngeal nerves to chemoreceptors in the medulla.
- Chemoreceptors communicate with medullary cardiac and vasomotor centres which:
- Increase firing via sympathetic nerves to increase heart rate
- Decrease vagal stimulation
- Increase sympathetic stimulation of blood vessels- vasoconstriction
What is the main way that the stroke volume can be increased?
Which law can be applied here?
Through increasing preload
Starling’s Law: the more a muscle is stretched, the more powerfully it will contract.
What affects preload?
Ventricular filling, which is influenced by:
- Heart rate
- Ventricular compliance
- Central venous pressure, which is influenced by:
- Venous compliance
- Thoracic venous blood volume
- Total blood volume
- Venous return
- Respiration
- Muscle contraction
- Gravity
- Atrial contractility
What is the effect of ventricular hypertrophy on preload?
Reduced preload as hypertrophy reduces compliance as muscles fibres do not stretch as much.
What is Starling’s Law?
What occurs with ventricular overload/myocardial injury?
The more a muscle is stretched, the harder it will contract.
- Therefore: increased end diastolic volume (preload) will lead to increased stroke volume.
Ventricular overload/ myocardial injury (from increased preload or afterload) = long term adverse remodelling:
- Ventricular hypertrophy and decreased compliance = decreased end diastolic volume → decreased stroke volume
