Cardiovascular System - Paper <=1998

Back to homepage

1998 – 2^nd semester Q1_Part_A

The initiation of a cardiac impulse is due to the unstable membrane potential expressed by the auto rhythmic cells situated near the entry of the vena cava. These cells are called pacemaker cells and they fire spontaneously without input from the nervous system and there are located within the sinoatrial Node of the right atrium.

These cell membranes of these cells display decreased exit of potasium ions and an increased entry of sodium ions because they unstable state of the ion channels. This causes electrical imbalance between the interior and exterior of the cell and as a result the membrane potential is decreased and this fires up the opening of the calcium ion channels forcing calcium to enter the cells. Thus the depolarisation of the fiber's membranes is caused. This depolarization wave is conducted along the entire atrial walls through the intercalated discs but not as of yet in the ventricles. This is because of the separation between the atria and ventricles by the presence of some connective tissue. When the impulse reaches the atrioventricular node which is the only point of connection between the two functional different compartments, the atria have already contracted therefore forcing blood into the ventricles. The fibres of the AV node are smaller in diameter and as a result there is a small delay and this enables for the atria to fully contract before the ventricular fibres are excited and contracted. 

The impulse is then conducted along with interventricular septum, through the Bundle of his. This then splits into two pathways, a left and right pathway. The impulse travels along these pathways and then excites the purkinje fibres located within the myocardium of the heart wall. The excitation of these fibres causes the contraction of the myocardial fibres and therefore the systole. Notably, the Papillary muscles are the first to be innervated by the these Purkinje fibres because this ensures that the AV node is shut before ventricular contraction occurs therefore not allowing blood enter back into the atria of the heart.

Major Points: Autorthymicity & how a depolarisation wave is generated , The mechanisms of delay & synchronous contractions, Cardiac impulse generation, Conduction of impulse, Significance of papillary muscles contracting before any other muscle

1998 – 2^nd semester Q1_Part_B

Heart rate is controlled by several factors but the main stimuli is the parasympathetic and sympathetic fibres of the autonomic nerve system. The parasympathetic fibres (particularly from the right chain) have a inhibitory effect on the heart rate. The heart’s inherent firing rate determined by the pacemaker cells of the SA node is about 80-100 beats per minute. But due to the vagus nerve having a tonic breaking effect on the cardiac muscle cells acting via acetylcholine receptors, the resting heart rate is below that of the inherent level – 60-80 beats per minute. Increased vagal influence, beyond that of normal levels will cause bradycardia.

Heart rate can also be controlled by the sympathetic division of the autonomic nervous system and this is by the cardiac accelerator nerves. These nerve act via b1 noradrenergic receptors to reduce the threshold potential of the muscle fibres and therefore allowiing for threshold to be reached more readily. This causes a greater level of heart rate. Increased levels of cardiac accelerator nerve activity will cause tachycardia.

 Heart rate is also controlled by many other factors highlighted briefly below.

v   An increase in temperature will cause an increase in heart rate because of the increased cardiac output in order maintain body temperature.

v    Increased stretch of SA node fibres causes increased preload and hence increased heart

v    Increased levels of circulating adrenaline increased heart rate and also causes more thyroid hormone to be present in the blood circulation

v    Increased levels of co2 build up in tissues will cause increased levels of heart rate due to more oxygenated blood required at the tissues

v    Decreased oxygen levels in the body will bring about increased heart rate pumping more blood to the lungs to be oxygenated and delivered to the tissues. This is also coupled with an increased ventilation rate.

v     Increased levels of potassium and calcium ions will have an inhibitory effect of heart rate.

 Major Points: Parasympathetic stimulation, Sympathetic Stimulation , Other factors also affect the HR

1998_2^nd semester_Q2

The answer can be found here. 

1997_2^nd semester_Q1_Part_A

An essay format answer can be found here.

Major points here: Fibrous Pericardium & Serous Pericardium & Visceral and Parietal Layer & Percardial Cavity & Pericardial Fluid à Epicardium (Visceral Layer) & Myocardium (cardiac muscle) & Endocardium (squamous cells + loose connective tissue).

1997_2^nd semester_Q1_Part_B

Ventricular filling occurs after systole where most of the blood from the ventricles is ejected into the associated blood vessels: namely the pulmonary trunk and aorta.

The period of ventricular filling occurs after a period of isovolumic relaxation. This is immediately after systole, when the AV valves and the semilunar valves are closed and some blood is left behind in the ventricles after ventricular contraction. When the pressure within the ventricles drops below that of the atria, the AV flaps “unseal” and open to allow a rapid rush of blood to enter into the ventricles. This is the first factor in ventricular filling. The second step is characteristerised by the slow filling of the ventricles when blood enters the atria and then continues into the ventricles as the valves are still open. The final phase of ventricular filling involves the contraction of the atrial walls, squeezing out the last drop of blood into the ventricle. By this time, the ventricles are ready to contract and the AV valves have shut due to back pressure applied by ventricular blood.

The end diastyolic volume is referred to the volume of blood present in the ventricles just prior to ventricular systole. This accounts to about 120-130ml. The end systolic volume of blood refers to the amount of blood present after systole has occurred. This is about 20-30ml. The amount of blood ejected into the aorta and the pulmonary trunk is the stroke volume, and is defined as the difference between EDV and ESV. Thus if this is a large value, then we would expect more blood to be entering the pulmonary and systemic circulations and therefore increasing cardiac output. When stroke volume is low, sometimes due to hindered venous return, the cardiac output is affected and is also low.

1995_2^nd semester_Q2_Part_A

The basic structural plan of most blood vessels is that they contain three main layers namely: tunica intima, tunica media and tunica adventitia. The tunica intima is composed of the endothelial layer of squamous epithelial cells and their associated basement membrane, and also some loose connective tissue. The tunica media is composed of circular bundles of smooth muscle and some elastic tissue and the tunica adventitia is composed mainly of collagen fibres, and this may have its own blood supply in some of the larger blood vessels, called d vasa vasorum.

In terms of the arterioles, the basic plan here is that they have a large proportion of their walls made of muscle. This is smooth muscle, and is richly innervated by the postganglionic fibres of the sympathetic division of the autonomic nervous system. These vessels are always under a partial contracted state known as vascular tone, and this enables them to regulate intraluminal pressure therefore they are referred to as resistance vessels. There is little or no tunica adventitia.

The basic structure of the a non-fenestrated capillary is somewhat different. This is because capillaries normally only have a wall consisting of simple squamous epithelium, their associated basement membrane and sometimes some loose connective tissue. Unlike arterioles, there is no muscle, nor tunica adventitia composed of collagen fibres. These vessels are the smallest type of blood vessels and are normally associated with capillary networks (capillary beds).

Major points: Three main layers of a blood vessel, What layers are evident in arterioles as opposed to capillaries.

1995_2^nd semester_Q2_Part_B

The extrinsic mechanisms involved in controlling blood flow to a region or a tissue are: neural regulation and hormonal regulation. Neural regulation involves the sympathetic division of the autonomic division of the nervous system.

The smooth muscle surround blood vessels especially arterioles are richly innervated by sympathetic fibres, mostly of the postganglionic variety. These release noradrenaline from their terminal ends. As the smooth muscle have an excess of alpha adrenergic receptors, the noradrenaline binds to these and then causes intense vasoconstriction. This increases the resistance and decreases blood flow. Also fibres releasing acetylcholine will bind to smooth muscle fibres around blood vessels supplying skeletal and cardiac muscle regions, and cause vasodilation or relaxation of the muscle. This will increase the blood flow. Also the arterioles are always under some form of constriction due to the vascular tone, which is due to the rich innervation of this smooth muscle.

The other type of control is the hormonal regulation. Adrenaline released from the adrenal medulla can reinforce the effects of noradrenaline by binding to the apha receptors of smooth muscle cells and cause vasoconstriction. Also they bind to non-innervated b2 receptors present in muscle cells surround bv’s of skeletal muscle and cardiac muscle region, this cause vasodilation and hence increases blood flow. Also Vasopressin (ADH) is indirectly involved in blood flow because it is a vasoconstrictor of blood vessels, therefore decreasing blood flow.

Major points: Neural Regulation & noradrenaline, apha adrenergic receptors & vasoconstriction , Acetyl choline & cholinergic response results in vasodilation, Vascular tone , Hormonal regulation & adrenaline, non-innervated b2 receptors & vasodilation, ADH effects?

1995_2^nd semester_Q1_Part_B

The heart contains two types of valves. The atrioventricular valve between the two atria and the ventricles and the semilunar valves (entry point of the aorta and the pulmonary trunk). The semilunar valves are names: aortic and pulmonic valves respectively.

The structure of the atrioventricular valves is different to that of semi-lunar valves. The atrioventricular valves are made of cusps which seal off against pressure from the blood. The right AV valve is made up of three cusps and is called the tricuspid valve whereas the left AV node is made up of two valves and is called the Bicuspid valves. These cusps are distally attached to tendon like structures called chordae tendone. These tendon like structures are further attached to muscles projecting out of the ventricular myocardium, called papillary muscles. It is these muscles which contract first upon reaching of the cardiac impulse and tense the chordae tendinae which seals off the cusps upon back pressure from the blood fill of the ventricles. The cusps allow for the closing of the valves and are functionally relevant during ventricular contractions, preventing backflow of the blood into the atria. The blood flow is always from the atria to the ventricles, thus these valves act as unidirectional valves.

 The semilunar valves are made of crescent shaped cusps which project out from the walls of the major blood vessels associated with the heart. There is no chordae tendonae. These cusps act as flaps which open when blood puts pressure on one side during ventricular systole. These are unidirectional valves, allowing blood to flow only from the ventricles into the blood vessels.  

Clinically two heart sounds can be heard using the ascultatory method. The first heart sound represents the closure of the AV valves denoting onset of systole. The second heart sound represents the closure of the semilunar valves, denoting the onset of diastole.