Control of Heart Function Flashcards
What are the 3 systems that control heart rate?
- CNS
- Renal system
- Blood vessels
How does the CNS affect heart rate?
What does the CNS have?
What are its actions and how does it control HR?
The CNS affects the HR via the ANS - composed of the sympathetic and parasympathetic branches
A cardio-regulatory centre and vasomotor centres in the medulla
PNS activates ‘rest and digest’ by reducing HR, SNS activates ‘fight or flight’ by increasing HR and force of contraction (inotropy)
PNS is activated majority of the time, SNS only activated when excited / exercising etc.
PNS works by lengthening phase 4 / decreasing the slope of phase 4, SNS works by shortening phase 4 / increasing the slope of phase 4
SNS activation results in more APs in the SAN cells
What does the action potential of an SAN cell look like?
Draw the curve on the graph below:
What is meant by the terms chronotropy and inotropy?
Chronotropy = change HR by altering electrical conduction system e.g. SAN impulses
Inotropy = alters the force of muscular contractions
How does the renal system increase HR?
Is there both, SNS and PNS activity to the kidneys?
How do these NSs affect the kidneys to affect the heart?
ANS regulates the kidneys, which goes on to regulate the HR
There is no PNS activity to the kidneys, only SNS
SNS activation increases BP by affecting the renal system - reduces glomerular filtration rate (GFR), so less Na+ goes into the tubular system of the kidneys (in the filtrate), so less water follows (decreased osmosis), which increases blood volume
SNS activates renin, angiotensin II, aldosterone system - kidney increases renin release, which increases Angiotensin II release = potent vasoconstrictor = increases BP
What is found in the cardiopulmonary circuits? And where specifically are they found?
How do these sensors in the blood vessels help control BP?
Volume sensors, a type of baroreceptor - present in the large pulmonary vessels, atria and right ventricle. They sense changes in volume and act accordingly
In the cardiopulmonary circuit, when it detects a reduction in volume (derease in filling), it decreases baroreceptor firing, which activates the SNS. When it detects an increase in volume, the distension increases baroreceptor firing, which inhibits SNS activity / increases PNS activity
Arterial circuit = ontrains pressure sensors
Increase in pressure = increases baroreceptor activity
What is found in the arterial circuit? And where specifically are these found?
How do these sensors help control BP?
Contain baroreceptors (pressure receptors) - located in the aortic arch, carotid sinus and the arterioles of the kidneys
If they detect a reduction in pressure, baroreceptor firing also reduces, which increases SNS activity
And if they detect an increase in pressure, baroreceptor firing increases so SNS activity is inhibited / decreased
What is the ANS? What type of neurons do the SNS and PNS contain? What is found in the synapses of these neurons?
Which ANS branch innervates the heart, and which the circulation system?
PNS contains short pre-ganglionic fibres that activate the post-ganglionic fibres using ACh release. Post-ganglionic fibres act on muscuranic (M2) receptors of the heart also using ACh. Important for controlling heart rate
SNS contains longer pre-ganglionic fibres, also releasing ACh to act on the nicotinic receptors of the shorter post-ganglionic fibres. Post-ganglionic fibres act on noradrenergic receptors using noradrenaline. Important in controlling blood circulation
What is meant by the terms chronotropy and ionotropy?
Chronotropy = increase in HR
Ionotropy = increase in contractility / force of contraction
Where is the vasomotor centre (VMC)?
How does the VMC function?
What are the 3 main parts the VMC is composed of?
What are the 2 different portions of the VMC and what do they each influence?
The VMC is located in the medulla and lower third of the pons and is part of the ANS
Many different areas of the brain control the VMC, such as the hypothalamus, etc. The hypothalamus controls HR by the hormones it releases. The VMC transmits impulses to the blood vessels via the spinal cord
- Vasoconstrictor - pressor
- Vasodilator - depressor
- Cardio-regulatory inhibitory area
Lateral portion - has its affects on HR via the SNS, affects HR and contractility
Medial portion - has its affects via the vagus nerve (PNS activity) to decrease HR
How does the brain affect the heart?
What receptor does the SNS act on and what is that receptor linked to, increasing what activity?
What receptor does the PNS act on and what is that receptor linked to, decreasing what activity?
Both ANS branches go to the SAN
SNS increases SAN activity via Beta-1 receptors - associated with G-S (S = stimulatory) linked proteins that activate adenyl cyclase, which increase cAMP activity and protein kinase A, increase HR
PNS acts on the M2 muscuranic receptors on the heart on the SAN - associated with G-I linked (I = inhibitory) proteins, which reduce adenyl cyclase and cAMP activity, reduce positive impact on chronotropy decreasing HR
What happens if SNS activity is removed?
What happens if PNS activity is removed?
What occurs if both branches are removed and why?
If SNS nerves were cut off = small reduction in HR
If PNS nerves were cut off = increase in HR
If both were cut off = increase in HR
There is underlying tonic (continuous) activity of both the SNS and PNS, however, the PNS is more active under tonic conditions (restful conditions)
How is blood volume and BP detected by the body?
How do the kidneys increase blood volume and so consequently BP?
How can BP be increased?
Blood volume = venous volume receptors, BP = arterial baroreceptors
Decrease in glomerular filtration = decrease in Na+ excretion = increase H2O reabsorption in the kidneys
Increased renin production and secretion = increased angiotensin II production = vasconstriction
What is GFR?
What are the 2 main ways the renal system is impacted by the SNS?
What is the name of the receptor they act on and how does it lead to reduced Na+ excretion?
What are juxtaglomerulus cells and what is their function? How it is impacted by the SNS?
Glomerular filtration rate
SNS affects afferent arteriole more than the efferent arteriole. SNS activity results in a release of noradrenaline, acting on the alpha-1 adrenoceptors causing vasoconstriction of both arterioles, but more in the afferent arteriole. Less blood enters the glomerulus and bowmans capsule, decreasing GFR so less Na+ is filtered out / excreted
Juxtaglomerulus cells located around the afferent arterioles, and are the site of renin synthesis, storage and secretion. SNS activates these cells via noradrenaline acting on the beta-1 adrenoceptors - more renin secretion and so angiotensin II production = vasoconstriction
What does the cardiopulmonary circuit predominantly contain, and what does the arterial circuit predominantly contain?
Cardiopulmonary circuit = large pulmonary vessels = volume sensors, arterial circuit = aortic arch, carotid sinus, afferent arterioles of the kidneys = pressure sensors
Which system (arterial or venule) contains more blood?
Why is the cardiopulmonary system more important with volume regulation?
What does constriction in the veins result in?
What does constriction in the arteries result in?
Vein and venules contain greater volume of blood than the arterial system
As the amount of blood flowing back to the heart determines the preload, impacting cardiac output (less preload = less CO)
Constriction in the veins = reduced compliance in the veins = less blood goes back to the heart (redued preload)
Constriction of arterial system = increases blood pressure (increased afterload)
What is a mechanism to regulating blood flow?
What are the 2 types of mediators?
What are the names of the 4 most common local mediators in the blood?
What are the names of the 5 most common systemic mediators in the blood?
Via mediators in the blood
- Local - mediators released from the blood vessels themselves (usually from the endothelial cells of the blood vessels) and can be broken down into vasodilators or vasoconstrictors
- Systemic - hormonal systems not produced within the endothelial cells of the blood vessels and can also be broken down into vasodilators and vasoconstrictors
Common local mediators - nitric oxide and prostacylin (vasodilators), Thromboxane A2 and endothelins (vasoconstrictors)
Common systemic mediators - Kinin and ANP (vasodilators), ADH and noradrenaline/adrenaline and angiotensin II (vasoconstrictors)
How do the cardiac action potentials differ from the nervous action potentials? Any why?
What are the 5 phases of the cardiac AP? Label them on the graph below and describe them:
Last much longer (100x longer) - long slow contraction = effective pump
The 5 phases are labelled 0-4:
0 = upstroke, depolarisation of the membrane, going from a non-excitable state to an excitable state leading to contraction
1 = early repolarisation, membrane potential begins to become more negative
2 = plateau, repolarisation plateaus, important for generating the force of the contraction = prolonged contraction
3 = repolarisation, membrane potential becomes more negative
4 = resting membrane potential, membrane potential reaches rest at -70mV
What are the different types of APs in different parts of the heart?
Caused by different ion currents flowing and different ion channel expression in the heart
Mainly the nodal cells that have a more different AP
What are the 3 phases of the SAN?
How does the AP in the SAN different? (HINT: how is the upstroke different)
What is a ‘funny’ current?
Phases 0, 3, 4 (no early repolarisation or plateau), 0 = upstroke, 3 = repolarisation, 4 = pre-potential (no longer named RMP as they do not stay resting for long)
Upstroke is no longer dependent on VG Na+ channels, instead AP is primarily generated via VG Ca2+ channels = Transient-type (transient = faster)
‘Funny’ current = activation of Na+ current, for slow depolarisation during phase 4 (pre-potential)
