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.
Describe the response of the cardiovascular system to standing up
-When you stand blood pools in the superficial veins of the legs due to gravity -Central venous pressure falls and causes cardiac output to fall (less going in) -Arterial and venous pressure are now falling -Baroreceptors detect falling arterial pressure and increase the HR -Total peripheral resistance increased to increase venous pressure
How does a pacemaker cell repolarise?
Efflux of K+ ions
How do class III anti-arrhythmic drugs (Block K+ channels) work? Give an example of one of these drugs.
Prolong the action potential, by blocking K+ channels (responsible for repolarisation). The absolute refractory period is lengthened, preventing another AP from occurring too soon. Amiodarone
How does angina occur?
When O2 supply to the heart does not meet its need. Ischemia of the heart tissue leads to chest pain, usually on exertion and relieved by rest. It is due to narrowing of the coronary arteries (atheromatous disease)
How does the cerebral circulation meet the high demand of oxygen?
-High capillary density -High basal flow rate -High extraction rate
How does vasoconstriction occur?
Located in the outer tunic adventitia are unmyelinated nerve endings. Sympathetic nerve fibres stimulate vasoconstriction by releasing noradrenaline at the nerve endings and diffuses through fenestration in the external elastic lamina into the external tunica media to depolarise some of the superficial smooth muscle cells. Depolarisation is propagated to all cells of the tunic media via gap junctions.
How is hypoplastic left heart syndrome caused?
If part of the endocardial tube gets pinched shut in a region that becomes the future ventricle, hypoplastic heart syndrome will occur.
How long is the QRS complex normally?
0.12s (3 squares) or less
How does the elastic nature of arteries acts to reduce arterial pressure fluctuation between systole and diastole?
Arteries have distensible walls, allowing them to stretch in systole. More blood flows in than out, so pressure does not rise so much. The arteries recoil in diastole and flow continues through the arterioles.
How is a secure cerebral blood supply created?
-Structurally - anastomoses between basilar and internal carotid artery -Functionally - brainstem regulates other circulations, myogenic autoregulation and metabolic factors
How might drugs be used to treat hypertension?
Drugs used in the treatment of hypertension act to reduce cardiac output and/or peripheral resistance. For example ACE-inhibitors, diuretics, adrenoceptor blocks and calcium channel blockers.
If there was no parasympathetic or sympathetic activity acting on the heart what would be the intrinsic heart rate? Why is the resting heart actually 60bpm?
100bpm however, the resting as there is lower as there is more parasympathetic activity acting on the heart than sympathetic
How would you work out the average pressure?
Diastolic pressure plus 1/3rd pulse pressure (Systole is shorter than diastole)
In pacemaker cells what causes the gradual depolarisation of the cells?
The funny (If) current carried by Na+ ions via slow Na+ channels that open as the potential goes very negative (repolarisation)
In the pulmonary circulation what pressures are found in the arteries and veins?
Arterial 12-15mmHg Venous 5 mmHg Capillaries in the middle
In the lungs what effect does an increase in the capillary pressure have on lymph?
More fluid to leave, oedema forming.
Is hypoplastic left heart syndrome compatible with life?
Without intervention this can be lethal.
List the five types of acyanotic heart defect.
-ASD -PFO -VSD -PDA -Coarctation of the Aorta
List the four types of cyanotic heart defect.
-Tetralogy of fallot -Tricuspid atresia -Transposition of the great arteries -Hypoplastic left heart
State some specific features of cardiac muscle
-Striations -Branching -Centrally positioned nuclei (1 or 2 per cell) -Intercalated discs -Adherens-type junctions -Gap junctions -The T tubules of cardiac muscle are inline with the Z bands and not with the A-I band junction
What are after-depolarisations?
Abnormal depolarisations following the action potential, thought to be caused by high intracellular Ca2+ (leads to longer QT interval)
Suggest why an arrhythmia might arise?
-Ectopic pacemaker activity -After-depolarisations -Re-entry loop (normal spread disrupted by damaged area)
Other than their diuretic action what other action do ACE inhibitors have?
Prevent the formation of the vasoconstrictor angiotensin II, thus promoting vasodilation of arterioles and venous dilation. This decreases both afterload and preload to the heart.
Suggest some vasodilators to increase capillary recruitment and vasodilation of capillaries.
-Adrenaline acts on B2 receptors causing vasodilation -K+ -Increased osmolarity -Adenosine -Inorganic phosphates -H+
What are inotropic drugs?
Drugs that affect the force of contraction of the heart
What are pericytes?
These cells are capable of dividing into muscle cells, or fibroblasts during angiogenesis, tumour growth and wound healing
What are the four abnormalities of tetralogy of fallot?
-VSD -Overriding aorta -Pulmonary stenosis -Right ventricular hypertrophy
What are the three layers of a blood vessel called?
-Tunica Intima – Next to the lumen -Tunica Media – Intermediate -Tunica Adventitia – Outer layer
What are the four basic classes of anti-arrhythmic drugs?
-Drugs that block voltage gated Na+ channels -Antagonists of β-adrenoceptors -Drugs that block K+ channels -Drugs that block Ca2+channels
What are the two circulations in the lungs?
-Bronchial -Pulmonary
What are the two heart sounds created by?
S1 - mitral and tricuspid S2 - aortic and pulmonary
What are the two layers which make up serous pericardium?
-Parietal layer (outside layer - next to fibrous) -Visceral layer (inner layer - adheres to heart)
What are the two types of resistance vessels?
-Arterioles -Pre-capillary sphincters
What are the ways used to reduce the workload of the heart in angina?
-β-blockers -Ca2+ channel blockers -Organic nitrates
What are vasa vasorum? Where are they found?
Translated as “vessels of vessels” - little blood vessels that supply the big ones. They are found in the Tunica Adventitia of the vessels.
What are VSDs?
VSDs are an opening in the interventricular septum (most commonly the membranous portion of the septum) can occur at any point. Since left ventricular pressure is much higher blood flows from left to right.
What conditions might cause an increased risk of thrombus formation?
-Atrial fibrillation -Valve disease
What can chronic hypoxia in the pulmonary circulation lead to?
-Increase in vascular resistance -Chronic pulmonary hypertension -Right ventricle pumps harder -Right ventricular heart failure
What conditions might cause an increased risk of thrombus formation?
-Atrial fibrillation -Valve disease
What conditions might first degree heart block be a sign of?
-Coronary artery disease -Acute rheumatic carditis -Digoxin toxicity -Electrolyte disturbances
What does coarctation of the aorta result in?
The narrowing of the aorta increases the afterload on the left ventricle and can lead to left ventricular hypertrophy.
What diuretic action do ACE inhibitors have?
Prevents release of angiotensin II and therefore prevents release of aldosterone from the zona glomerulsa. Usually aldosterone causes water retention, increasing blood volume so reducing it decreases blood volume and decreases pre-load to the heart.
What diuretic action do ACE inhibitors have?
Prevents release of angiotensin II and therefore prevents release of aldosterone from the zona glomerulsa. Usually aldosterone causes water retention, increasing blood volume so reducing it decreases blood volume and decreases pre-load to the heart.
What does coarctation of the aorta result in?
The narrowing of the aorta increases the afterload on the left ventricle and can lead to left ventricular hypertrophy.
What does increasing the tube do to the flow rate?
The middle layers move faster so the mean velocity of flow also increases
What does increasing the tube do to the flow rate?
The middle layers move faster so the mean velocity of flow also increases
What factors oppose vasomotor tone?
Vasodilator factors (H+, K+ and Adenosine)
What factors oppose vasomotor tone?
Vasodilator factors (H+, K+ and Adenosine)
What happens to the flow rate when the viscosity of a fluid is increased?
The middle layers will slow down so the mean velocity of flow decreases
What happens to the flow rate when the viscosity of a fluid is increased?
The middle layers will slow down so the mean velocity of flow decreases
What happens to the pacemaker potential to decrease the heart rate? How does this occur?
Makes the pacemaker potential less steep by acetylcholine acting on M2 receptors.
What happens to the pacemaker potential to decrease the heart rate? How does this occur?
Makes the pacemaker potential less steep by acetylcholine acting on M2 receptors.
What happens to the pacemaker potential to increase the heart rate? How does this occur?
Makes the pacemaker potential more steep by noradrenaline targeting a2 receptors.
What happens to the pacemaker potential to increase the heart rate? How does this occur?
Makes the pacemaker potential more steep by noradrenaline targeting B1 receptors.
What is a paradoxical embolism?
A PFO can be the route by which a venous embolism reaches the systemic circulation if pressure on the right side of the heart increases even for a minute.
What is a paradoxical embolism?
A PFO can be the route by which a venous embolism reaches the systemic circulation if pressure on the right side of the heart increases even for a minute.
What is a patent ductus arteriosus?
It is the failure of the ductus arteriosus to close. This is a vessel that exists in the foetus to shunt blood from the pulmonary artery to the aorta before the lungs are functioning. It should close shortly after birth as the pressure in the pulmonary artery drops following perfusion of the lungs.
