Control of heart function Flashcards
- What can the 3 main anatomical components of the heart be broadly categorised as?
- Muscle cells (cardio-myocytes): can contract and relax in response to electrical stimuli. Essential for pumping blood around the body
- Specialised electrical cells: cells that create spontaneous currents and those that transmit currents exist within the heart. Essential for regulating contraction of the cardio-myocytes
- Vessels: the major blood vessels are responsible for transporting blood in and out of the heart, whilst the coronary blood vessels are responsible for supplying blood to the heart
- What is the pacemaker of the heart?
- Where is the pacemaker of the heart located?
.
Sinoatrial node - usually beats at around 60-100bpm.
Junction of the crista terminalis; upper wall of right atrium and opening of the superior vena cava
- Where is the AV node located?
- What tract connects the SAN and AV nodes?
Triangle of Koch at the base of the right atrium.
(Has pacemaker activity with a slow calcium mediated action potential: but it is usually the SAN that controls the heart beat).
Internodal tracts, which are specialised myocytes.
- What is the pathway of the bundle of His in the heart?
From the atria
on to the bundle of His
down through the intraventricular septum
to the bundle branches
then through to the actual Purkinje fibres
which propagate the electrical current along the ventricles.
- How many phases does nodal AP have and name each of them?
3
Phase 4 - Pre-potential Phase 0 - Upstroke Phase 3 - Re-polarisation
- Outline the process of a nodal AP
Pre-potential (phase 4) → Na+ influx through a ‘funny channel’- Increase in membrane potential from -60 to -40 mV
Upstroke (phase 0) → Increase in membrane potential -40 to 0 mV due to Ca2+ influx Re-polarisation (phase 3) decrease in membrane potential due to K+ efflux
- What causes the different action potential profiles in the different parts of the heart?
Different ion currents flowing and different ion channel expression in the cell membrane
so different parts of heart have different action potential shapes
- Is a cardiac muscle AP longer than a nervous AP? How long is a cardiac muscle AP?
- What does duration of a cardiac muscle AP control?
Yes
Cardiac muscle AP - 200-300 ms
(Nervous - 2-3ms)
Duration of contraction of the heart
- How many phases are present in a cardiac muscle AP and name each phase?
5
Phase 0 - Upstroke (-90 mV up to ~20-30 mV) → Na+ influx Phase 1 - Early re-polarisation → Decrease in Na+ permeability Phase 2 - Plateau (maintains cell at a level of depolarisation at value of 0mV) → Due to Ca2+ influx Phase 3 - Re-polarisation → Happens at ~270ms after stark of upstroke → K+ efflux Phase 4 - Resting Membrane Potential - Na+/K+ ATPase pump
- What is the absolute refractory period of a cardiac muscle AP?
- What is the relative refractory period of a cardiac muscle AP?
- What 2 components are important for control of the heart via the CNS?
Time during which no other AP can be initiated regardless of stimulus intensity
First 200ms
Period after ARP where an AP can be elicited, but only with larger stimulus strength. Cardio-regulatory centre and vasomotor centres in medulla.
- What affect do the 2 different components of the ANS have on the heart and how they affect action potential curve
Parasympathetic (goes via vagus nerve to the heart)
When activated it causes a decrease in HR
decreases the slope of phase 4 OF SAN potential (pre-potential nodal AP phase)
Therefore reduces HR
Sympathetic
increased HR
by increasing the slope of phase 4 of SAN potential (decrease in time of phase 4)
increase in force of contraction, increases Ca2+ dynamics.
- What is chronotrophy?
- what is ionotrophy?
factors changing speed of heart rate
factors changing force of heart rate
- Where do parasympathetic nerves arise from?
- Describe the design of the parasympathetic response in terms of what is released at the pre and post-ganglionic nerve fibres
Craniosacral outflow (cranial and sacral part of the spinal cord).
Pre-ganglionic fibres use ACh as NT. Use nicotinic receptors Post-ganglionic fibres also use ACh as a NT. Use muscarinic receptors,
- Where do sympathetic nerves arise from?
- Describe the design of the sympathetic response in terms of what is released at the pre and post-ganglionic nerve fibres
Thoracolumbar outflow.
Pre-ganglionic fibres use ACh as their NT; use nicotinic receptors. Synapse at sympathetic ganglia. Post-ganglionic fibres use noradrenaline, use adrenergic receptors (where post-ganglionic fibres are longer than pre-ganglionic fibres).
- Where is the vasomotor centre located?
- What is the vasomotor centre composed of?
Bilaterally in reticular substance of medulla and lower third of pons.
Vasoconstrictor (pressor) area Vasodilator (depressor) area Cardio-regulatory inhibitory area
- Give an example of a part of the brain that can exert powerful excitatory or inhibitory effects on the VMC
- What do the lateral and medial portions of the VMC control respectively?
- How does it transmit its impluses?
Hypothalamus
Lateral - influences HR and contractility Medial - Signals via Vagus nerve to heart that tend to decrease HR
Distally through spinal cord to almost all blood vessels
Outline the process of parasympathetic cardiac innervation
Releases ACh which act on M2 muscarinic receptors;
G-I linked proteins (inhibitory) reduces levels of cAMP and adenylyl cyclase activity
Reduces impact on positive chronotropy
HR decreases
- Outline the process of sympathetic cardiac innervation
Released noradrenaline
Increased activity of Beta-1 receptors associated with G-S linked proteins
activating adenylyl cyclase,
increasing activity of cAMP and protein kinase A- Secondary messenger signalling pathways
cAMP activated by Beta-1 receptors, essential to molecular regulation of ion channels, influences of HR and contractility
Sympathetic innervation is linked with cAMP intracellular concentrations
- What happens if you cut the parasympathetic nerves to the heart?
Heart rate increases due to sympathetic activity
Larger effect on heart rate than if the sympathetic nerves were cut
- What effect does sympathetic innervation have on the renal system and how does this affect cardiac function?
Decrease glomerular filtration and decrease sodium excretion
increase in blood volume as water moves in (aldosterone)
detected by venous volume receptors
Sympathetic nerves also increase renin secretion
increases angiotensin II production
causes vasoconstriction and increase in blood pressure
which is detected by arterial baroreceptors
So the kidneys affect cardiac function by having an impact on blood volume and blood pressure
- What effect does sympathetic innervation have on the renal system and how does this affect cardiac function? (think chronotrophy and inotrophy)
decreased chronotrophy as increased pressure detected by baroreceptors will cause decreased SNS activity which decreases heart rate
increased chronotrophy as increased blood volume so increased force of contraction in heart
- What effect does sympathetic innervation have on the afferent arterioles of the glomerulus and nephron tubule cells?
Primary site of sympathetic activity
The sympathetic activity causes vasoconstriction
they release noradrenaline
acting on alpha-1 adrenoceptors and activating them
causing vasoconstriction
results in a reduction in glomerular filtration rate and a reduction in the amount of Na+ filtered
Release of renin from the juxtaglomerular cells by beta-1 adrenoceptor activation, which subsequently increases aldosterone, which increases blood volume
- What is the cardiopulmonary circuit?
- Explain how the cardiopulmonary circuit reacts when there is a decrease in filling in the heart
Large pulmonary vessels that are volume sensors (also atria and right ventricle): send signals through glossopharyngeal and vagus nerves.
Decrease in filling leads to decreased baroreceptor firing leading to an increase in sympathetic nerve (SNS) activity This increases the HR
- What is distention?
- Explain how the cardiopulmonary circuit responds to distention
State of being enlarged due to internal pressure (in terms of the heart it is when the heart is full - caused by more blood coming back to the heart)
Distention leads to an increase in baroreceptor firing. Leads to a decrease in sympathetic activity.
- What is the arterial circuit?
- Explain how the arterial circuit responds to a decrease and increase in pressure
Consists of aortic arch, carotid sinus and afferent arterioles.
Pressure sensors - also send signals through glossopharyngeal and vagus nerves.
Increase in pressure → Decreased baroreceptor firing leading to increased SNS activity. Decrease in pressure - Increased baroreceptor firing leading to decreased SNS activity.
- What is the venous volume distribution affected by?
- Which circulation accounts for most of the volume of blood circulating in the human body?
Peripheral venous tone, gravity, skeletal muscle pump and breathing
Venous volume (systemic blood flow) - 61%
- What is the central venous pressure?
- How does constriction of veins affect compliance and venous return?
- what is compliance?
Mean pressure in the right atrium- determines swelling of heart
Constriction reduces compliance and increases venous return.
compliance is used to describe how easily a chamber of the heart or the lumen of a blood vessel expands when it is filled with a volume of blood
- What does arteriole constriction determine?
Blood flow to downstream organs
Mean arterial blood pressure The pattern of blood flow to organs
- What is difference between the local and systemic mechanisms of regulating blood flow?
Local - intrinsic to smooth muscle; important for reflex local blood flow regulation within an organ.
Systemic - extrinsic to smooth muscle; include Autonomic Nervous System and circulating hormones
what are examples of endothelium derived mediators?
Nitric Oxide- Vasodilator- diffuses into vascular smooth muscle cells
Prostacyclin- Vasodilator- has antiplatelet and anticoagulant effects
Thromboxane A2- Vasoconstrictor- synthesised in platelets
Endothelin- Vasoconstrictor- generated from nucleus of endothelial
what are examples of non endothelium derived mediators?
Kinins: bind to receptors on endothelial cells & stimulate NO synthesis – vasodilator effects
Atrial natriuretic peptide (ANP): secreted from the atria in response to stretch – vasodilator effects to reduce BP
Vasopressin (ADH): secreted from pituitary gland. Binds to V1 receptors on smooth muscle to cause vasoconstriction
Noradrenaline/Adrenaline: secreted from adrenal gland (& SNS); causes vasoconstriction
Angiotensin II: potent vasoconstrictor from the renin-angiotensin-aldosterone axis. Also stimulates ADH secretion.
