Cardiovascular System

Question 1

Orientation of the Heart

Answer 1

Right atrium: Right border 
Right ventricle: Inferior border 
Left ventricle: Left border 
Great vessels: Superior border 
Apex of the heart points anteriorly and inferiorly.

Question 2

Structure of pericardium and heart wall

Name the layers and their properties

Answer 2

From outermost to innermost
Fibrous pericardium: Made of collagen-protective capsule.
Parietal pericardium: Made of mesothelial cells to form a serous membrane.
Pericardial Cavity: Sac of serous fluid which reduces friction and provides protection against mechanical shock.
Visceral pericardium: The other side of the pericardium.
Myocardium: Layer of muscle making up the contractile layer of the wall. Consists of cardiac muscle.
Endocardium: Layer of endothelial cells. Provides smooth surface for lower resistance to blood flow.

Question 3

Fibrous Skeleton of the heart

Position and function

Answer 3

Full rings around the mitral and aortic valves. Half ring around tricuspid valve.
Provides a strong frame for valves to attach to for support against high pressures generated by systole. Prevents overstretching of valves.
Acts as an electrical insulator. Prevents APs in the atrium from reaching the ventricle except through the delaying AV node.

Question 4

Ventricular Filling

Outline actions carried out by chambers and approximate pressures/volumes

Answer 4

Ventricular filling: Passive movement of blood from atria to ventricles. All pressures around 0. Accounts for nearly 80% of blood entering ventricles.
Arterial pressure gradually decreases as the blood drains into branches of the artery.
Lasts around 500ms.

Question 5

Atrial ejection (Outline actions carried out by chambers and approximate pressures/volumes)

Answer 5

Contraction of atria to force last 20% of blood into ventricles. Not necessary for survival. Pressure increases slightly to around 20mmHg. Inefficient as there are no valves to prevent backflow into the veins.
Lasts around 250ms.

Question 6

Isovolumetric ventricular contraction (Outline actions carried out by chambers and approximate pressures/volumes)

Answer 6

Pressure of ventricles increase from ~0mmHg to 80mmHg. Volume does not change as mitral valves to cause the first heart sound (lub). Deep in tone as the valve is large.
The pressure in the aorta at the end of this step is known as the diastolic blood pressure.

Question 7

Ventricular Ejection (Outline actions carried out by chambers and approximate pressures/volumes)

Answer 7

Quiet opening of aortic valves once ventricular pressure exceeds 80mmHg. Systole continues up until a maximum pressure of 120mmHg. The pressure gradually decreases back down to 100mmHg due to inability of ventricle to contract any harder. Aortic pressure varies in a similar pattern.
During this time, atrial pressure increases as blood is being emptied into it.
For the right ventricle, the pressure only increases to about 30mmHg.
Lasts around 400ms
The maximum pressure attained during this phase is the systolic pressure, and is used to indicate cardiac health.

Question 8

Isovolumetric Ventricular Relaxation (Outline actions carried out by chambers and approximate pressures/volumes)

Answer 8

Ventricular pressure rapidly decreases. Aortic and pulmonary valves close and cause the second heart sound. Slightly disjoined as the aortic valves close slightly earlier due to higher pressure.
As blood rushes against the aortic valves, pressure temporarily rises then falls again in a DICROTIC wave.

Question 9

Structure and function of Elastic Arteries

Answer 9

Large arteries which received blood ejected by the ventricles.
Contains many sheets of elastin in its tunica media to allow it to stretch when pulses of blood are pumped into it- high compliance. Recoil gradually pushes blood into the branches. Smooths out blood flow.

Question 10

Structure and function of Muscular arteries

Answer 10

Contains tunica externa, media and intima with defined boundaries. T.M is thicc and made of smooth muscle. Muscles in the wall can contract and control radius to control blood flow and pressure to ensure that blood is delivered at high enough pressure.

Question 11

Structure and function of arterioles

Answer 11

Small lumen and thickest relative smooth muscle tunica media layer. Has constant smooth muscle tone. Highest pressure drop and resistance to flow as to avoid damage to capillaries. Contracts to reduce pulsatility of blood flow. Controls total peripheral resistance and mean blood pressure.

Question 12

Structure and function of capillaries

Answer 12

Thin 9 micrometer wide vessels with only a one-endothelial-cell-thick tunica intima. Slow blood flow and thin walls allows exchange of materials to occur via diffusion. Blood plasma pushed out into tissuebed by pressure then reenter bu osmosis.
No CT or smooth muscle so very susceptible to surges in pressure.

Question 13

Structure and function of venules

Answer 13

Has tunica externa and intima, and occasionally a
thin tunica media of smooth muscle. Larger lumen, high distensibility of walls and low pressure to allow efficient draining of capillaries. Leaky walls allow extravasation of WBCs during an immune response.

Question 14

Structure and function of veins

Answer 14

Large lumen vessels with pliable walls containing elastin. Walls hence expand readily to accomodate increase in volume of blood- allows veins to act as reservoir.
Venoconstriction allows more blood to enter the arterial half of the circulation. By reducing the volume accomodated by the veins, it forces more blood into the arterial half of the circulation.
Delivery of blood at low pressures. Has valves to prevent backflow of blood.

Question 15

Classification, location and role of Coronary Arteries

Answer 15

Muscular arteries branching off the aorta downstream of the aortic valve- valves direct backflowing blood into these arteries. These vascularise cardiac myocytes and are drained by cardiac veins.
Blockage of these by atheroma causes atherosclerosis, where the walls of the vessels encroach the lumen and cause narrowing (minimum of 20% of lumen area occlusion). Can cause ischemia.
Left coronary artery supplies ventral left and minority of dorsal. Right coronary artery supplies ventral right and majority of dorsal.

Question 16

Preload- What affects it/consequences

Answer 16

Preload: Increasing end diastolic volume will stretch myocytes more. They will hence contract with greater force-Frank/Starling’s Law of the Heart.
Increases with increasing venous return, blood volume, venous compliance (which increases venous return) and duration of ventricular diastole (varies with heart rate). Increasing heart rate slightly will reduce preload, but increase in contractility will counteract the reduction.
Venous return varies with the effectiveness of:
-respiratory pump: pressure gradient which can draw blood upwards towards the heart.
- muscular pump: contractions of skeletal muscles which can push blood along veins.
- Blood volume.
- Venoconstriction- smooths out walls of veins and reduces resistance to flow.

Question 17

Describe how heart rate is controlled by the nervous system.

Answer 17

Initially the rate is controlled by the rate of depolarisation at the SA node-around 90-100 per minute. Parasympathetic innervation by the CHOLINERGIC Vagus X cranial nerve reduces this to 60 per minute.
Detection of blood pressure by baroreceptors in the aortic arch and the carotid sinus provides the sensory stimulus for a reflex arc-connected to the CNS via the glossopharyngeal nerves.

Question 18

Describe the Cardiac Action Potential.

Answer 18

p(Na+) is high initially, causing significant depolarisation from -90mV to 20mV.
Ca2+ channels open and maintain the action potential at around 10mV. (This still counts as depolarisation). Presence of Ca2+ enables contraction- contraction phase.
K+ channels open after around 200ms

Question 19

Describing Cardiac Electrical Activity/Conditions with an ECG

Answer 19

ECG measures electrical activity at the skin’s surface at many different leads/lines planes of view.
Depolarisation of the atria form the p-wave, which is a small bump. Followed by a flatline which represents atrial diastole.
The QRS complex represents ventricular depolarisation and contraction. Followed by another flatline representing ventricular diastole.
Finally, there is a long, drawn out peak representing ventricular repolarisation.
Larger P and R waves represent enlargement of the atria and ventricles respectively.
Larger Q-waves represent myocardial infarction.
Smaller T-waves represent insufficient oxygen, while larger T-waves represent excess K+.

Question 20

Starling’s Law of Capillaries

Answer 20

The promotion of filtration is due to BHP while the promotion of reabsorption is due to BCP. They have roughly equal and opposite effects, leading to an equilibrium of fluid movement across the whole capillary.

Question 21

Pressures involved in driving capillary exchange.

The equation for net filtration pressure.

Answer 21

Blood hydrostatic pressure/ BHP: Caused by physical pressure of blood pushing liquid out against walls. Varies with vasoconstriction /vasodilation/gravity. Directed out.
Blood colloidal pressure/BCP: Osmotic pressure brought about by albumens in the blood reducing water potential there and drawing water in by osmosis. Directed in.
Interstitial fluid hydrostatic pressure. Small hydrostatic pressure due to pressure of interstitial fluid. Directed in.
Interstitial fluid colloidal pressure: Small osmotic pressure brought about by the small amount of albumens in the I.F. Directed out.

NFP= (BHP+IFOP)-(IFHP+BCOP)

Question 22

Factors affecting Blood Flow and Poiseuille’s Law

Answer 22

Poiseuille’s Law: rate of flow is proportional to the radius to the fourth power.
Increasing radius hence increases rate. Parallel arrangment of vessels also increases the ‘radius’ available for blood to flow through, hence increasing rate.
Related: If vasoconstriction occurs in one vessel, parallel arrangment allows increased bloodflow through other vessels as the blood must go somewhere else.
Increasing surface area reduces rate of flow, as it provides a larger surface over which friction can occur. Hence, blood flow in capillaries is the slowest due to the highest SA.

Question 23

Equation of Blood Pressure

and why it is regulated.

Answer 23

BP= TPR x CO
TPR= (Mean Arterial Pressure x Central Venous Pressure)/ Cardiac Output
Regulation ensures constant and suitable environment for exchange. Excess pressure= damage. Insufficient pressure= Inefficient.

Question 24

Sources of Sensory Input for Blood Pressure and Regulation and their mode of action.

Answer 24

Baroceptors in the carotid sinuses and the aortic arch.
Cardiopulmonary receptors in the walls of major veins which detect stretching.
They both deform and send sensory potentials to the cardiovascular centre of the medulla oblongata via the glossopharyngeal nerves.
Proprioceptors in vessels detect exercise, while chemoreceptors detect changes in blood composition.
Blood pressure can be regulated by input from higher brain centres eg: hypothalamus.

Question 25

Responses to Maintain Blood Pressure/ MAP

Hormonal

Answer 25

NEGATIVE FEEDBACK MECHANISM
Renin-Angiotensin-Aldosterone system acts in response to hypovolemic shock.
Renin is produced by juxtaglomerular cells in response to SNS stimulation by the CV centre, as well as in response to the stretching of juxtaglomerular cells. It stimulates Angiotensin I production from the liver and conversion to Angiotensin II with ACE in the lungs. These stimulate vasoconstriction to increase TPR, It also stimulates Aldosterone release, which drives the reabsorption of water to retain blood volume.
ADH acts similarly to aldosterone by increasing the expression of aquaporins, as well as acting as a vasopressin to increase vasoconstriction.
Atrial natriutic peptide is synthesised in the atria and stimulates Na+ and water excretion at the kidneys, which reduces blood volume.
Renal responses such as the RAA are hormone mediated, so they are long lasting and slow.
Nitric Oxide is released by paracrine signalling and causes vasodilation.

Question 26

Responses to Maintain Blood Pressure/ MAP

Autonomic Nervous

Answer 26

Effectors controlled by SYMPATHETIC INNERVATION act quickly, between 2-3 heartbeats.
SNS innvervation of adrenal medulla stimulates increased secretion of norepinephrine and epinephrine. Leads to increased norepinephrine activity on A-1 receptors of smooth muscle in walls of arteries.
SNS stimulation of the myocardium increases inotropy and hence CO. Uses norepinephrine (excitatory) which targets the B-1 receptors on cardiac myocytes in the myocardium and the SA/AV nodes.
Similarly, catecholamines and epinephrine bind to B-1 receptors on cardiomyocytes to similar effect.
Increases CO and TPR (by constricting vessels)
Vagal axons innervate also the cardiac myocytes and SA nodes, and act in opposition to the cardiac accelerator nerve. Uses acetylcholine which binds to muscarinic receptors. Has minimal effect on cardiac myocytes as there are few muscarinic receptors.
High frequency of vasomotor innervation of blood vessel smooth muscle leads to vasoconstriction and vice versa.

Question 27

Afterload- What affects it/Consequences

Answer 27

Afterload: Increasing pressure in the elastic artery means more pressure is needed to overcome the arterial pressure. Hence, less blood is pumped out and end diastolic pressure increases to increase preload.
Varies with changes in arterial pressure and diameter.
Afterload changes leads to preload changes- increasing afterload means less blood is pumped out. More blood remaining= more EDV.

Question 28

Inotropy- What affects it/ consequences

Answer 28

Contractility/inotropy: Increase ability of myocytes to contract. Can be affected by hormones, sympathetic innervation- beta receptors for norepinephrine or other chemicals such as extracellular Ca2+ concentration.

Question 29

Structure and Function: Foramen ovale/ Fossa Ovalis

Answer 29

Hole between the left and right atria, which is covered by a flap of CT on the left atrium side.
Pulmonary circuit in a foetus tends to have very little blood due to the high pressure in the lungs. Left ventricle hence would atrophy. Foramen ovale allows some blood to flow into the left ventricle so it can pump.
Postnatally, the high pressure in the left side of the heart (due to functional pulmonary circuit) pushes on the CT flap and closes it.
Patent foramen ovale results in additional blood entering the pulmonary circuit via the right atrium.

Question 30

Structure and Function: Ductus arteriosus/ Ligamentum arteriosum

Answer 30

Duct of smooth muscle from the branches of the pulmonary trunk to the aorta. Used to shunt blood from the high resistance pulmonary circuit to the systemic circuit (foetal circulation is a 1-circuit system)
Postnatally, blood can no longer be shunted through as the resistance in the pulmonary circuit is lower. The ductus arteriosus will constrict to become the ligamentum arteriosum.

Question 31

Structure, Location and Function: Moderator Band

Answer 31

A band made of modified Purkinje muscle fibres that short circuits the cardiac conduction system so the cardiac potential reaches the apex first. Coordinates contraction so blood is pushed up more efficiently.
Found only in the right ventricle.

Question 32

Factors affecting Cardiac Output

Answer 32

• Increased venous return due to increased blood volume, contractility and venoconstriction. This increases preload
• Increased sympathetic innervation via the cardiac accelerator nerve, or epinephrine/norepinephrine hormonal stimulation. Leads to increased heart rate and SV.
• Reduced Parasympathetic activity via the vagus nerve. Reduces heart rate.

Question 33

Factors affecting Systemic Vascular Resistance

Answer 33

Increased number of red blood cells increases viscosity- blood flows less easily (polycythemia)
Increased body size increases total length of blood vessels and hence increased total surface area.
Decreased blood vessel radius due to vasoconstriction or atherosclerosis. Vasoconstriction is brought about by activation of A1 receptors by norepinephrine/epinephrine.

Question 34

Role and structure of Atrioventricular valve and associated structures

Answer 34

Tricuspid on the right and mitral (bicuspid) on the left.
They attach to the fibrous cardiac skeletons, which prevents them from overstretching.
Mitral valves have significantly larger papillary muscles, and are anchored by far more chordae tendineae.

Question 35

Structure of Aortic/Pulmonary valves, and ways they can be damaged.

Answer 35

Three cup shaped cusps which inflate when blood attempts to backflow. Cusps fit together to form tight seams.
Damage to it can be due to antibodies produced during rheumatic fever. Damages collagen and disrupts the seamlike structure. Leaves a permanent gap in valve structure.
Reduces valve lumen so ventricles need to contract harder which leads to hypertrophy. Gap also allows backflow of blood causing a murmur.

Question 36

How does Vasoconstriction increase blood pressure?

Answer 36

Reducing the size of the lumen increases resistance and lowers flow. Causes accumulation of blood upstream of the vasoconstricted section. Blood exerts a greater force in order to push itself through the vessel.

Question 37

How does venoconstriction increase blood volume?

Answer 37

Venoconstriction reduces reservoir volume so less blood can be stored. Constriction also reduces surface area so the resistance increases and blood flow increases and blood passes through more easily into the arterial circulation.

Question 38

Effect of Vasoconstriction of Peripheral arterioles and Conditions when that Occurs.

Answer 38

Occurs during hypovolemic shock to maintain blood flow and high blood pressure in the key organs.
Vasoconstriction increases resistance and reduces blood flow into the vessel, resulting in blood accumulation upstream of the vessel which increases pressure in the upstream vessel. Reduced blood flow therefore means pressure is reduces.
The accumulated blood can flow to other core organs which maintains the volume of blood there.

Question 39

Effect of Vasoconstriction on Upstream, Downstream and the affected vessel.

Answer 39

Vasoconstriction increases resistance of the vessel and blood flows through the vessel less readily. Increased volume of flood increased force exerted on the walls of the upstream vessel, so pressure there increases.
The reduced blood flow through the downstream vessel means the pressure downstream is reduced.