Cardiac Output and HR control Flashcards
What is CO?
How is it calculated? (and its components)
Cardiac output (CO) is the volume of blood pumped by each ventricle per minute
- Not the total amount of blood pumped by the heart
CO = HR x SV
- HR = bpm
- SV = volume of blood ejected per contraction/volume of blood pumped by each ventricle per heart beat = (EDV - ESV in ventricle)
What are the typical figures for EDV, ESV, SV, HR and CO for the adult at rest?
For adult subject at rest,
- EDV about 135mL
- ESV about 65mL
- Therefore SV at rest c. 70mL
- HR for adult at rest is around 70bpm
- So CO is 4900 mL/min = 4.9L/min = rounded out to 5L/min (from each side of the heart)
How is CO controlled?
How do HR and SV vary across fitness levels?
CO is controlled according to physiological requirements
- Via control of HR and SV
Fitter individuals have lower HR (50bpm) but higher SV (105mL)
How is SV controlled intrinsically?
What is this called?
What is the relationship called (and the governing law)
Why is this not a simple relationship?
SV can be controlled intrinsically
- By increasing venous return - preload
- EDV increases
- The length-tension relationship of cardiac muscle: Frank-Starling Law of the heart (instrinsic reln btwn EDV and SV)
- greater cardiac muscle stretch due to greater EDV increases the force of the cardiac contraction
- increases SV without any nervous system input to the heart
- This is not a simple reln bc the heart does not eject all the blood it contains.
Describe the length-tension reln of skeletal muscle and cardiac muscle
What is the molecular anatomical basis governing this relationship?
The length tension relationship of skeletal muscle and cardiac muscle are similar:
For skeletal muscle, tension generated in contraction depends on the amount of the overlap between thick and thin filaments
- resting muscle length gives maximum tension when it is stimulated to contract
- Shortened or stretched muscle (before muscle stimulated to contract) yield lower tension (too much or too little filament overlap)
Cardiac muscle normally only operates in the ascending limb of the length-tension curve
- y axis SV rather than tension/x axis EDV
- So if increased EDV (preload) stretches cardiac muscle to above resting length, the tension generated in contraction increases and the SV increases
What are the advantages of the Frank Starling law of the heart?
Advantages of the Frank Starling law of the heart:
- Equalizes output btwn left and right sides of the heart: blood pumped equally distributed between the pulmonary and systemic circulations
- When a larger CO is required, e.g.during exercise, venous return is increased through action of the sympathetic NS. The resulting increase in EDV automatically increases SV.
What factors control the SV extrinsically?
What is the effect?
What is it called?
What is the mechanism?
SV is subject to extrinsic control by
i) sympathetic stimulation and
ii) adrenaline (reinforces effect of symp stimulation via noradrenaline)
Both enhance the heart’s contractility (strength of contraction at any given EDV) - this is called inotropic action. - i.e. SV increases without an increase in EDV (FS surve shifts upwards)
This increased contractility is due to increased Ca2+ entry into the cell triggered by NorAd/Ad.
What are preload and afterload?
How much pressure must a heart generate to eject blood?
Preload: EDV (extent of filling) referred to as preload bc it is the workload imposed on the heart before contraction begins
Afterload: Arterial blood pressure referred to as afterload bc it is the workload imposed on the heart after contraction begins
- Ventricular contraction pressure must exceed arterial BP in order to force the semilunar valves open
What is normal BP?
What happens to a person with sustained increased BP?
What are downsides of this?
Normal bp = 120/80 mm Hg systolic BP/diastolic BP
For individuals with high BP, over time the heart starts to enlarge (muscle mass increases to counteract the increased pressure required).
Downsides:
- A diseased or weakened heart may not be able to compensate completely, leading to heart failure.
- In an enlarged heart, the space for filling in the ventricles with blood DECREASES. Leads to congestive heart failure
How is heart rate controlled intrinsically and extrinsically?
Name the types of extrinsic control of HR
How is this effected?
What is it called?
HR control:
Intinsic: set by the depolarisation rate of the sinoatrial (SA) node.
Extrinsic: ANS influences on the SA node. The heart is innervated by both divisions of the ANS (even though nervous stimulation is not required to initiate contraction)
-
Sympathetic stimulation:
- Increases HR - Chronotropic Tachycardia (S&T)
- Increases contractile strength of myocardia muscle - Inotropic
- Parasympathetic stimulation: Decreases HR - Chronotropic Bradycardia (P&B)
ANS stimulation of the heart is effected by changing the slope of the pacemaker potential (of autorhythmic cells)
Changes in rate of pacemaker potential are called chronotropic effect.
Compare inotropic vs chronotropic action
Inotropic action: changes in contractility of heart muscle at any given EDV, i.e. (strength of contraction increases & FS curve shifts upwards)
Chronotropic action: changes in rate of pacemaker potential in autorhythmic cells i.e. (slope of pacemaker potential becomes steeper)
What neurotransmitters are involved in tachycardia and bradycardia?
Which receptors are involved?
What is the mechanism of action on the SA node and resulting effect on HR?
The parasympathetic NS ( via vagus nerve) releases acetylcholine ACh
- acts via muscarinic receptors
- Bradychardia (slows done HR) via: slows down depolarization rate of SA node and hyperpolarizes cell by increasing K+ permeability (slowing closure of K+ cells) - DONT HAVE TO REMEMBER THIS
The sympathetic NS releases noradrenaline (akanorepinephrine in USA)
- acts via β1-adrenergicreceptors
- Tachycardia (speeds up HR) via: speeds up depolarization rate of SA node by augmenting funny channels (Na+ entry) and transient channels (Ca2+ entry) - DONT HAVE TO REMEMBER THIS
What are the other effects of parasympathetic stimulation on heart activity (apart from decreasing HR by hyperpolarisation/decreasing rate of spontaneous depolarisation of SA node)?
Other effects of parasympathetic stimulation:
- Weakens atrial contraction: shortens plateau phase of atrial contractile cells AP
- Decreases AV node excitability: prolongs transmission of AP to ventricles so time between
- Little effect on ventricular contraction: ventricles not innervated by parasympathetic nerves
What are the other effects of sympathetic stimulation on heart activity (apart from speeding up HR via speeding up depolarisation of SA node)?
- Increased contractile strength of the atrial and ventricular contractile cells (heart beats more forcefully and squeezes out more blood) - inotropic action
- Speeds up relaxation
- Sympathetic stimulation of the AV node reduces AV nodal delay by increasing conduction velocity.
- Speeds up spread of the AP throughout the specialised conduction pathway: bundle of His and purkinje fibers
Therefore note: Hormone adrenaline and noradrenaline (from sympathetic fibers) (catecholamines)
- increase heart rate (chronotropic action) and
- force of myocardial contraction (inotropic action).
Define inotropic & chronotropic action
Are they extrinsic or intrinsic control?
- Inotropic action is the increase in contractile strength of cardiac muscles at any given EDV. It increases the SV and therefore CO. It is extrinsic control
- Chronotropic action is the change in slope/rate of pacemaker potential. It changes HR and therefore CO. It is extrinic control
- Tachycardia (HR increases)
- Bradycardia (HR falls)
Label the diagram
