Cardiovascular System Flashcards
To cover most aspects of CVS for ESA 2. This is only for revision purposes, you'll need to do your own stuff. Everything contained is may be shit, use at your own risk. Note: You will still need to go through vital signs, ECG prep and embryology.
Are arteries high resistance or low resistance vessels?
Low resistance
Define the term flow
The volume of fluid passing a given point per unit of time
Are arterioles high resistance or low resistance vessels?
High resistance
Define the term central venous pressure.
The pressure in the great veins supplying the heart
Define the term contractility.
. Contractility is not the force of contraction of the heart, rather the stroke volume you get for a given venous pressure
Define the term after-load on the ventricular myocardium
The force necessary to expel blood into the arteries
Define the term pre-load on the ventricular myocardium
When the ventricular myocardium is fully stretched and is exerting the same pressure as the venous pressure
Define the term velocity of flow
The rate of movement of fluid particles along the tube N.B. how far, nothing to do with volume
Describe the distribution of blood volume over the major parts of the circulation (arteries, capillaries etc.)
-11% (0.55 L) in the Arteries and Arterioles -5% (0.25 L) in the Capillaries -17% (0.85 L) in the Heart and Lungs -67% (3.35 L) in the Veins
Define the the term venous return.
The rate of flow of blood back to the heart.
Define the term stroke volume
The difference between end diastolic volume (amount left in after diastole) and systolic volume (amount left after systole)
Describe the response of the cardiovascular system to haemorrhage
-Large amount of blood is lost -Reduced venous pressure leads to decreased cardiac output and therefore low arterial pressure -Baroreceptors detects decreased arterial pressure causing HR and resistance to rise leading to further decrease in venous pressure -Need to sort out venous pressure soon
Describe the response of the cardiovascular system to eating a meal
-Increased activity of the gut leads to the release of metabolites and local vasodilation -The total peripheral resistance falls, causing the arterial pressure to fall and the venous pressure to rise. -The rise in venous pressure and fall in arterial pressure causes a rise in cardiac output and heart rate. -The extra pumping of the heart reduces venous pressure and raises arterial pressure
How can the inferior mediastinum be organised?
-Anterior mediastinum -Middle mediastinum -Posterior mediastinum
Explain what Starling’s law is…simply.
More you put in the harder it contracts. Harder it contracts, the higher the stroke volume.
How do class I anti-arrhythmic drugs (block voltage gated Na+ channels) work? Give an example of one of these drugs.
Na+ channels in the open/inactive state are blocked, but the drug dissociates quickly in time for the next action potential. As Na+ channels are blocked, after-depolarisations cannot trigger another AP. Lidocaine is an example.
How do class II anti-arrhythmic drugs (β-adrenoceptor antagonists) work? Give an example of one of these drugs.
Block sympathetic action by acting on β1 receptors in the heart, decreasing the slope of the pacemaker potential in the SAN. Inhibits adenyl cyclase, decreasing inotropy. (used after an MI) Beta blockers (propanolol, atenolol)
How do class IV anti-arrhythmic drugs (drugs that block Ca2+ channels) work? Give an example of one of these drugs.
Decreases slope of pacemaker action potential at SA node. Also decreases AV nodal conduction and decreases the force of contraction. (also causes some coronary and peripheral vasodilation) Drugs like verapamil
How does adenosine act and what does it do?
Acts on A1 (adenosine receptors, not a1 adrenoreceptors) inhibiting adenylyl cyclase at the AV node. Increases K+ conductance and hyperpolarises cells of conduction tissue. it is anti-arrhythmic and resets the heart.
How do organic nitrates work to treat angina?
Primary function - Venodilation to reduce the preload to the heart
Secondary function - Dilation of coronary arteries perfusing the heart more
They react with thiols (-SH groups) in vascular smooth muscle causing NO2- to be released. NO2- is reduced to NO, which is a powerful vasodilator.
How does NO (nitric oxide) work as a vasodilator?
-Activates guanylate cyclase -Increasing cGMP -Lowering intracellular Ca2+ to cause relaxation of vascular smooth muscle
How does excitation spread during systole?
- The SA node fires an action potential, which spreads over the atria causing atrial systole. The AP reaches the AV node, where it is delayed for about 120ms. 2. From the AV node, excitation spreads down the septum between the ventricles 3. Excitation spreads from inner (endocardial) to outer (epicardial) surface
How can the transposition of the great vessels be treated?
Initially a ductus arteriosus and/or an ASD can be maintained or created to allow for enough blood flow to support life. From this a full repair can take place, reconnecting the correct arteries.
How does the distensibility of blood vessels allow for blood flow to be increased?
Diameter of the lumen increases, so resistance falls and flow increases.