Cardiovascular Function and dysfunction

The following information is taken from my university lecture notes. I will add extra information (as I learn more on my own). Will also have to clean it up because its messy at the moment.

WARNING: THIS NOTE IS HUGE AND MESSY!

Functions of Cardiovascular system:
- maintains adequate blood flow to all body tissues
- rapid-transport system for gases, specialized cells, nutrients and waste
- keeps blood pressure within normal limits
- provides rapid adjustment to changes in demand
- temperature and fluid regulation

Structure of the heart

Neural Connections

Structure of the heart:
- Right atrium and ventricle = right pump => pulmonary circuit
- Left atrium and ventricle = left pum => systemic ciruit
- Atria and ventricles separated by connective tissue ring
- Heart wall consists of four layers (Peri-, Epi-, Myo-, Endo - cardium)
- Myocardium consists of striated branched cells with intercalated discs = ''functional syncytium''
- Energy efficient tissue

Microanatomy:
- Short fat branching cells
- One large central nucleus per cell
- Intercalated discs
- Gap junctions
- Myofibril-like units
- High capillary density
- Large number and size of mitochondria
- Large sarcoplasmic reticulum and T.Tubule system

Electrical activity of the heart:
- Conduction system = specialized cells that initiate and distribute electrical impulses to ''contractile'' cells
- Sinoatrial (SA) node contains pacemaker cells that establish the heart rate (across atria). Connects to atrioventricular (AV) node via 'internodal' pathways. The impulse travels down the bundle of His and splits into right and left bundle branches. The impulse is then distributed rapidly by Purkinjie fibres to ventricular muscle.

Mechanical events:
- Cyclical contraction (systole) and relaxation (diastole) relating to emptying and filling periods.
- Total time = 0.8s   of which Systole = 0.3s, Diastole = 0.5s

Heart Simulation link: the pressure and volume changes over the duration of a complete cardiac cycle. Normal blood volume is 5-6 litres. The rate blood volume circulates the body is measured by the cardiac output.
Cardiac output: is the volume of blood (ml or L) pumped out of the left ventricle per minute.
                   Stroke volume(ml/beat) x Heart rate (beats/min) = Cardiac output (l/min)
    During Rest/Exercise       80/100                        75/150                                6/15      
Cardiac output distribution at rest and exercise:
          Brain = 14%    14%      Heart = 4%   5%      Skeletal muscle = 21%   60%      Skin = 5%    15%    Kidneys = 20%   2%       Liver and GIT = 27%   2%     Other = 9%    2%
Factors affecting heart rate:
- Normal pacemaker activity = 80-100 b/min
- Parasympathetic decreases HR = 70-80 b/min:  via acetyl choline (ACh) acting on SA node cells
- Sympathetic increases HR via Norepinephrine (NE) acting on SA node cells
- Hormones epinephrine, thyroxine increase HR
Factors affecting Stroke volume
- The Frank-Starling principle: an increase in end-diastolic volume results in a greater stroke volume = increased ventricular filling causes increased ventricular stretch and causes increased contractile force. In other words, ''more in = more out''
- Sympathetic stimulation of receptors in cardiac muscle by norepinephrine (NE) from nerve fibres and epinephrine (E) from adrenal gland.
- Parasympathetic stimulation of SA and AV nodes by acetyl choline.
- Glucagon and thyroid hormones

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NOW THAT WE KNOW SOME BITS ABOUT CARDIOVASCULAR PHYSIOLOGY LETS TALK ABIT ABOUT BLOOD PRESSURE



Organisation of the circulatory system

Vessel            
Arteries ~4mm; (function=)distribute blood under high pressure to internal organs.
Arterioles ~30um; change in response to local, nervous or endocrine stimulation          
Capillaries ~8um; permit efficient exchange between blood and other mediums
Venules ~20um; collect blood from capillary beds
Veins ~5mm;  transport blood with the aid of valves

Arterial blood pressure:
- Blood Pressure (BP) is the pressure exerted by the blood against a vessel wall and it depends on the volume of blood and the resistance within the vessel. The volume of blood entering and leaving the arteries is not constant during heart contraction (systole) and relaxation (diastole). BP is separated into systolic (high) and diastolic (low). Systemic BP is greater than pulmonary BP.

Normal values
Systemic Arterial:
   Systolic BP=120mmHg
   Diastolic BP=80mmHg
Pulmonary Arterial
   Systolic BP=25mmHg
   Diastolic BP=8mmHg

Mean Arterial Pressure (MAP) = Diastolic + (0.33*(Systolic-Diastolic))
    e.g. 80 + (0.33* (120-80)) = 93mmHg (93mmHg is a normal MAP)





Control of BP and flow
- Blood flow through tissues depends on the pressure gradient and vascular resistance. Blood flows from high to low pressure down a pressure gradient (higher gradient=increased flow). Changes in diameter of arterioles affects blood flow and blood pressure. Blood pressure inceases when the diameter of arterioles decreases and vice versa

Control of blood pressure

 Decrease in blood pressure => causes decrease stimulation of baroreceptors => medulla cardiovascular centre => decrease parasympathetic stimulation of the heart => increase sympathetic stimulation of heart, arterioles, veins => increase in blood pressure


Factors affecting blood pressure: blood volume, heart rate, stroke volume, blood viscosity, peripheral resistance

Mean arterial pressure is determined by
  Cardiac Output x Total Peripheral Resistance

i.e. Blood pressure increases when:
- blood volume increases and/or
- Heart rate increases  and/or
- Stroke volume increases and/or
- Blood viscosity increases and/or
- Peripheral Resistance increases and/or

THE FOLLOWING WERE TAKEN FROM SECOND YEAR 

Lecture 1. The structure of the Cardiovascular System:

Review of functions and structure of cardiovascular system. Structure of heart. The layers of the heart, special properties of the myocardium, pressure differences in different chambers of the heart. Blood, brief overview of its constituents. Structural and functional differences between different blood vessels. Microcirculation. Differences between capillaries and lymphatic vessels, oedema.

Heart- General structure: It is located in the middle mediastinum of thorax; the apex of the heart is at the level of the fifth intercostal space; size of average fist. 

4 chambers, 2 thin atria, 2 thick ventricles (LV= 8-10 mm, RV= 2-3 mm); the atria are separated by the interatrial septum whilst the ventricles are separated by the interventricular septum. It contains valves between regions, e.g. AV valves (2 flaps-tricuspid on the right side and bicuspid on the left side) and also semilunar valves (3 flaps). The flaps are held by connective tissue called the chordae tendinae which are connected to the papillary muscles. Valves are passive and only move due to pressure changes.

Three layers are found in the heart, a thin endocardium (similar to endothelium of blood vessels), a thick myocardium and whole heart is enclosed in pericardium (thin fibrous sheath, with interstitial fluid as lubricant). The bulk of the heart is the myocardium, which  consists of cylindrically shaped muscle fibres with a rich supply of capillaries. The fibres are fused at regions called intercalated disks which allow a low resistance pathway for ion transport.

The contractile unit of the heart muscle is the sarcomere, which consists of myofilaments called actin and myosin which follow a sliding filament model of contraction. The tension developed by the cardiac muscle depends on the cross bridges between actin and myosin and thus the length of sarcomeres. As result of the tension generated during systole, blood is ejected from the heart to the aorta.

On each contraction of the heart, blood is expelled from the ventricles at high pressure (Systolic = 120 mmHg, diastolic= 80 mmHg) into the aorta and pulmonary artery. The expelled blood causes a rise in pressure in the aorta and distends its wall. During diastole the tension in the aortic walls maintains flow of blood onwards through the arteries, and the aorta diminishes in size until it is again distended at the next heart beat.

Blood flows around the system due to i) pressure difference ii) pumping of the heart iii) diastolic recoil of the arterial walls iv) compression of veins by skeletal muscles and v) negative pressure in thorax during inspiration.

Blood:e awvCVGBN

Our body fluids can be split into extracellular (outside the cells) & intracellular (inside the cells). The ECF can be split into the interstitial fluid (fluid not in the vascular system but baths the cells, 10.5L) and the blood (fluid in the vascular system, 3.5L). Blood is composed of red blood cells (40-45%) suspended in plasma (55-60%), and is a medium for transfer of heat, gases, proteins, glucose, waste products, fats, cellular debris. It is a complex fluid, whose properties and composition changes. Blood volume (RBC+plasma)= 5L, 70-75 ml/Kg body wt.; platelets= 2-3mm diameter, 150000-300000/mm³; WBC= 5000-10000/mm³; RBC= biconcave discs, diameter= 8mm, thickness=2-4mm, pigment Hb, 4.5-6 mill./mm³.

Also contains proteins (Albumin, Fibrinogen); electrolytes (Na⁺, Cl^-, K⁺, Ca²⁺); Cholesterol, triglycerides, urea, creatinine, glucose, uric acid. Produced in bone marrow by erythropoiesis.    

Transport System: The circulatory system is a closed system and can be divided into 2 circuits, the pulmonary and systemic.  The pulmonary circuit has less volume, vessels are shorter and thin walled and lower pressure and less resistance. The systemic circuit is a high pressure system and supplies and drains all the organs and tissues of the body. Length of vessels decrease from Aorta to venules, and then increase from terminal veins to vena cava. Thickness of vessels decrease and then increase and the no. also increase and then decrease. Velocity of blood is highest in aorta and decreases as the area of vessels in the body increases.

Arteries:

There are 2 types, elastic and muscular. The elastic predominate near the heart, whilst the muscular are more towards the end of the arterial tree. They have 3 layers separated by elastic membranes,

a) tunica intima- innermost layer, thin, surface of endothelial cells lying on a basement membrane b) tunica media- middle layer, thick, smooth muscle and elastic connective tissue c) tunica externa - fibrous connective tissue.

AORTA - large lumen, thick walls, pulsatile blood flow, systolic=120 mmHg, diastolic=80 mmHg

LARGE ARTERIES- elastic reservoir to store part of the energy of cardiac contraction

MAIN ARTERY BRANCHES/TERMINAL ARTERIES- to conduct blood to capillaries

ARTERIOLES- mainly smooth muscle, affected by local and circulating substances (vasoconstrictor and vasodilator), innervated by constrictor fibres mainly, main control of blood flow to organs,0.2-0.05mm diameter, supply 10-100 capillaries,main resistance to blood flow.

METARTERIOLES- smaller muscle-walled vessels, which feed into capillaries

Veins:Have larger diameter and thinner walls than arteries, easily distended,have smooth muscle, innervated by vasoconstrictor fibres, valves present in veins, except for smallest veins, venae cavae, veins from brain, portal system and pulmonary veins.

Blood reservoir- 55% of blood in systemic veins, 12% in heart, 18% in pulmonary circulation.

VENULES- 0.02-0.05mm diameter, outside layer of smooth muscle,controls outflow of blood from capillary bed

TERMINAL VEINS->MAIN VENOUS BRANCHES-->LARGE VEINS-->VENA CAVA (3 mmHg pressure, conduct blood back to heart)-->RIGHT ATRIUM

Physical factors affecting movement of blood:

Flow (volume/time) of blood is directly proportional to pressure and inversely proportional to resistance. Flow can be silent (no sound) or turbulent (noisy).

Flow=  (Pπr^4)/(8η1)   i am not sure about the equation please check this

Resistance:

The resistance to blood flow is affected by the length of vessels, the radius of vessels and the viscosity of blood. Changes of radius are the most critical in determining resistance and hence flow of blood. Arterioles are major sites of resistance

Viscosity:

Blood is 3-4 times as viscous as water. Plasma is 1.8 times as viscous as water. Viscosity in vivo is less than in vitro. An increase in the cellular composition of blood i.e haematocrit, increases viscosity , whilst anaemia leads to a decrease in viscosity. An increase in temperature leads to a decrease in viscosity and thus a decrease in resistance, whilst a decrease in temperature leads to an increase in viscosity. Increased viscosity will lead to increase work for the heart and thus possibly heart failure.      

Opening and closing of blood vessels:

The pressure inside blood vessels (distending pressure-P) must be balanced by the tension (T) on the outside walls of the blood vessels caused by the weight of tissues to prevent collapse or rupture. This is described by the law of Laplace (P=T/r, where r= radius). The smaller the radius, the lower T has to be to balance P. Thus capillaries despite their small size, don't rupture.

The microcirculation

capillaries, lymphatics, Starlings law, exchange of fluid, oedema

Consists of the capillaries and Lymphatic vessels.  The microcirculation has a large cross sectional area, thus low blood flow, its walls are very permeable and is adapted for exchange of water, gases, nutrients and waste materials.

Capillaries:

 Are short narrow tubes (10 billion capillaries, surface area= 500 m², one cell thick (1mm), up to 1mm long diameter= 7-10 um), which have a wall  made up of a single layer of endothelial cells plus a basement membrane. They do not have smooth muscle. Within the walls are slit like pores (50-90x10^-9 m. The capillaries in different parts of the body vary in their leakiness. Three main types can be distinguished i) Continous - found in nerve, skeletal muscle, fat and skin with very few pores ii)Fenestrated - found in intestines, endocrine organs and kidney these have small gaps iii) Discontinuous - found in liver, spleen and marrow, which have large intercellular gaps.

In areas such as the skin, ears and fingers there are shunts (Arteriovenous anastomoses), which are direct channels between the arterioles and venules, and are under nervous control (mainly constrictor fibres). Blood flow controlled by precapillary sphincters (minute bands of smooth muscle) and arterioles.

                                       

The function of the capillaries is exchange of substances. This is brought about by filtration, absorption and diffusion. These are determined by the leakiness of the walls, the capillary pressure and osmotic pressures according to the Starling model. Starling (1896) formulated the principles governing the exchange of fluid across capillaries. Three main factors were involved:

1/ Hydrostatic pressures- these are forces which tend to push fluid e.g. capillary blood pressure, interstitial (outside cells) fluid hydrostatic pressure

2/ Osmotic pressures- forces which oppose the pushing tendency of the hydrostatic pressures and are mainly caused by proteins e.g. capillary osmotic pressure  and interstitial hydrostatic pressure

3/ The conductivity of the capillary wall- the rate of transport of fluid across the capillary wall, which is affected by the area, distance across the capillary wall and viscosity of the fluid. Permeability varies e.g. very permeable in liver, spleen and bone marrow whilst practically impermeable in skeletal muscle

Both hydrostatic and osmotic pressures are on both sides of the capillary membrane, thus it is the difference in pressure across the capillary wall membrane which is important in exchange of fluid. If we consider the arterial end of the capillary, here the higher hydrostatic pressures favour filtration i.e. fluid leaks out into the tissue spaces. In the venule end of the capillary, the higher osmotic forces favour absorption from the tissue spaces i.e fluid leaks back into capillary. The balance of filtration and absorption may vary with changes in arterial tone. Capillary pressures on average are between 20-30 mmHg, however these pressures can vary widely depending on location e.g.s the glomeruli of the kidney= 60-70 mmHg; pulmonary capillaries= 7 mmHg.

Lymphatic system:

Is closely associated with the circulation, and are a series of thin walled vessels with valves that provided an alternative route for return of interstitial fluid, proteins, and fats via thoracic duct to venous system. The fluid that is returned is called LYMPH. Lymph nodes within the system filters lymph in removing bacteria and viruses. It has many valves and smooth muscle, and the fluid is propelled by external compression on lymph vessels by contracting muscles.

Lymphatic vessels:

Are porous, thin walled vessels resembling capillaries in all tissues except bone and central nervous system. Their function is to clear the interstitial spaces of excess fluid, proteins, lipids and foreign materials and return it to the vascular system. They are different from the capillaries in that their walls are attached to surrounding tissues thus preventing collapse and they are designed for entry of fluid. Large lymphatic vessels have muscular walls. The fluid that is carried in the lymph vessels is called Lymph, with a composition similar to plasma but with very little protein. The flow of this fluid is slow (2-4 L/day). The return of this fluid is made easier by compressing lymph vessels, by skeletal muscle contractions and by the presence of one way valves.

Oedema:

Is the accumulation of excess fluid in the interstitial (tissue) spaces of the body e.g. in feet, around eyes. It can be caused by 3 main factors i)Hypoproteinaemia- low plasma protein in capillary, thus greater outflow of fluid into the tissue spaces ii) Increased venous pressure, thus an increase in filtration from capillary and thus an increase in fluid in the interstitial spaces iii) Lymphatic obstruction- thus protein leaks from capillary lack of reabsorption of fluid.

Lecture 2. The cardiac cycle:

Definition of one cycle. Its importance. Electrical aspects of one cardiac cycle, pacemaker potentials and non-pacemaker potentials, the conductive tree and the ECG. Practical measurement of an ECG and its importance. Dysfunction: Arrythmias and heart abnormalities. Mechanical aspects of one cardiac cycle. Sounds and pressure changes in the aorta and left ventricle and their importance to blood pressure and cardiac output. Dysfunction: Heart failure.

The heart pumps blood for approx. 70 years. It has a weight of 300g for a man of 70 kg weight. The heart rate is 65 to 80 in resting man. At each heart beat 70-80 mls of blood is ejected into the aorta, known as the stroke volume.

The Cardiac Cycle

is the period (0.8 s) from one heart contraction to the next, started by the action potential from the sino-atrial node. It consists of 2 parts, diastole (period of relaxation- 0.5 s) and systole (period of contraction- 0.3 s). 

The importance of the cycle is twofold. 1/ It maintains blood flow for all the organs in the lifetime of the individual and 2/ Supplies the blood pressure to maintain the circulation.

Electrical events of the cardiac cycle:

To understand the mechanisms underlying contraction of cardiac, skeletal and smooth muscle we need to examine the structure and forces across cell membranes, particularly the membranes of nerves and muscles. In the 18th Century, it was noticed by the Italian, Galvani, that frog's legs twitched when they were hung on metal railings in a thunderstorm. But it was not until the 1940s and 1950s that the mechanisms underlying this twitching were elucidated. Hodgkin et al, using isolated Squid axons (large in size, easy to manipulate their structure), manipulated the concentrations of ions inside the axon and measured movement of these ions across the membrane (using radioactive isotopes). They found that the inside of the axon had a negative potential to the outside, there was mainly potassium inside and mainly sodium outside, and that nerve transport occurred when sodium entered the inside and set up a depolarising current (action potentials). Hodgkin and Huxley (1949), developed a technique called the 'Voltage Clamp Method' (a feedback method to hold membrane potential) to investigate the changes in membrane potential as nerve transport occurred.

 The next major advance occurred in the 1960s when chemicals were found to block action potentials. Tetrodotoxin (TTX) found in the 'Puffer fish' blocks sodium channels and causes paralysis and death. Tetraethylammonium (TEA) blocks the potassium channels. Both these blockers allow investigation of these channels.

 Neher and Sackman (1970s) developed a novel technique('Patch Clamp), by which individual ionic channels could be studied. Very fine glass micropipettes (diameter=um) literally grasps a single channel and measures the current flow through the channel. These channels conduct ions, they are selective, they function like gates or switches and thus control flow, they are differrent types of proteins. For example, the sodium channel is a single protein molecule (composed of 1800 amino acids) folded into 4 parts (but precise shape unknown), it is selective to only sodium and is voltage gated (opens or closes depending on the voltage).

Resting Potentials:

These vary depending on the type of tissue (e.g. muscle membrane=-90mV, blood cell membrane=-9mV). The value depends mainly on the concentration of sodium and potassium across membrane (Na+ outside = 145 mM; Na+ inside = 10 mM; K+ outside = 4 mM; K+ inside= 135 mM). However, the chloride ion (Cl-) also contributes. The concentration differences and the charges carried by the ions lead to chemical and electrical forces across the membrane. For each ion, the contributions these forces make to the resting potential can be calculated by using the Nernst equation (e.g. E_k=61.5 log₁₀ [K_o⁺]/[K_i⁺] at 37C, where E_k represents the voltage due to potassium ions,K_o⁺ and K_i⁺ are the concentrations of potassium inside and outside the membrane). Another equation which may be useful is the Goldman equation. The latter gives the size of the membrane potential at any given time for all the ions. The other determinants of the resting potential are the membrane permeability, and the active Na+/K+ ATPase (sodium-potassium pump) which pumps sodium out and potassium in.

Cardiac Muscle:

The cardiac muscle (myocardium) is striated (like skeletal muscle), muscle fibres consist of the proteins actin (thin, MW=42,000) and myosin (thick, MW=480,000). Cardiac muscle is a syncytium, i.e. the cardiac muscle cells are tightly bound together (actually there are 2 syncytiums, one for atria and the other for the ventricles). Each cell is 50-100 um long and 10-20 um wide. Between the cardiac muscle cells are intercalated discs (within which are gap junctions) which provide low electrical resistance and thus allow fast diffusion of ions and thus electrical activity. Skeletal muscle cells are isolated due to lack of these gaps. Stimulation of any single muscle fibre causes the electrical activity to travel over entire heart muscle. Cardiac muscle has the property of autorhythmicity, i.e. an external stimulus is not required to activate the cardiac cells. There is a delay of 10 ms for cardiac muscle between electrical activity and contraction (in skeletal muscle the delay is 2 ms). Cardiac muscle cannot be tetanised unlike skeletal muscle, nor can it fatigue.

The electric potential within a cardiac fibre is due to a semi-permeable membrane and the ionic composition inside and outside a cell. A value of -70 to -90 mV is commonly found. Resting potentials at the Sino Atrial node are lower (-40 mV).

The action potentials produced by depolarization (due to Na⁺ ions moving into cell), leads to release of Ca²⁺ ions which lead to contraction of cardiac muscle, followed by repolarization (K₊ ions moving into cell). The time course of this depolarization and repolarisation varies depending on the part of the heart.

Contraction of cardiac muscle occurs with myosin and actin forming crossbridges (sliding filament theory) in the presence of calcium. Relaxation is an active process (requires ATP) involving the rapid removal of calcium by ATPase and Cyclic AMP.

Conductive tree:

The action potential originates at the Sino-Atrial (SA) node (located at the junction of the Superior Vena Cava and the Right Atrium), travels across the atrial muscle, to the Atrio-Ventricular (AV) node (takes 66 ms), the Bundle of His (130 ms), then the right and left branches of the Purkinje fibres (260 ms). Speed is fastest in the purkinje system (5 m/s). The conduction through the AV node is slow (0.03-0.05 m/s) compared to atrial or ventricular muscle, to ensure that atrial contraction is completed before ventricular contraction begins. 

Cardiac action potentials:

The shape and durations of the action potentials generated along the conductive tree varies, but they can be grouped into two major types, pacemaker and non-pacemaker.

1/ Pacemaker:

These include those produced at the SA and AV nodes. Durations vary between 200-250 ms. The action potentials here are slow. The resting potential of these areas are between -40 to -60 mV, they are slowly depolarising constantly (upstroke due to combination of fall in K⁺ current, and rise in Ca²⁺ and Na⁺ currents) with very litle resting period, there is no plateau in the shape, and there is also a slow repolarisation (potassium currents). The pacemakers vary their discharge by 3 mechanisms, namely change in slope of depolarisation, changes in threshold potential for starting the action potential and the absolute value of the resting potential. The discharge rate is altered mainly by the autonomic nervous system (parasympathetic and sympathetic nerves) and circulating adrenaline. Parasympathetic nerves release Acetylcholine which slows the heart rate, whilst Sympathetic nerves release Noradrenaline which increases the heart rate. Adrenaline released from the adrenal medulla also increases the heart rate and force of contraction.

2/ Non-Pacemaker:

These are found in the atrial muscle, ventricular muscle (durations=250-300 ms) and the purkinje fibres (300-400 ms). The action potentials here are fast. The resting potentials here are much larger (-90 mV), there is a very rapid depolarisation (upstroke - due to rise in Na⁺ and fall in K⁺ currents); a rapid but short decline due to inactivation of fast Na⁺ current; a plateau (due to Ca²⁺ mainly and and slow rise in Na⁺⁾, and a repolarisation (due to K⁺,Ca²⁺ and Na⁺ currents). The shape shows a plateau, which allows action potential to last 10-30 times longer than in skeletal muscle, and thus increases the period of contraction. The reason for the plateau is a) large store of calcium and calcium influx continuous for 0.2 to 0.3 seconds i.e is prolonged b) immediately after start of action potential, there is a 5 fold decrease in potassium permeability of cardiac muscle membrane for 0.2-0.3 s which prevents repolarization of the membrane and thus contributes to plateau.

There is an absolute refractory period (200 ms) during which another action potential cannnot excite the cardiac cell. This is very important in allowing the ventricles to relax and refill with blood.

Measurement of E.C.G.:

Principle: As the action potential spreads across the heart and across the body, it can be viewed at any instant as an electric dipole (depolarised part being negative whilst polarised part is positive). An electrode placed on the skin can measure the change in potential produced by this advancing dipole. This forms the basis of the electrocardiogram or E.C.G.(a record of the electrical activity generated by the heart).

The E.C.G. can be recorded by measuring the potential difference between any two points on the body. These two points when taken together constitute a LEAD. The potential difference measured by the lead depends on the size of the electric dipole (wave of electrical depolarization), the direction of the electrodes and the distance of the electrodes from the dipole. The E.C.G. is normally recorded at a paper speed = 25mm/s and a gain or vertical deflection of 1 mV=10 mm. A full E.C.G. recording is made up of 12 leads. 6 leads record the electrical activity in the vertical plane (head to foot), whilst the other 6 leads (chest), record in the horizontal plane (across the chest).

Einthoven in 1903 developed the first practical device for recording cardiac potentials, called the string galvanometer, which became the Electrocardiograph. He developed the classical limb lead system, whereby an electrode is placed at each corner of an imaginary equalateral triangle superimposed on the front of a person (known as Einthoven's triangle). The three corners represented right arm (RA), left arm (LA) and left leg (LL).

Lead I was a recording of the cardiac potentials between RA and LA.

Lead II = recording between RA and LL.

Lead III = recording between LA and LL.

Einthoven's law- Lead I + Lead III = Lead II

Wilson in 1934, developed a further system, which amplified the action potentials, known as the Augmented (a) lead system (leads 4,5 and 6) called aVr (right arm), aVl (left arm) and aVf (foot).

Components of the E.C.G. trace:

P wave: atrial depolarisation, duration=0.1 s, height=< 2.5mm or 0.2mV

P-R interval: conduction time over the atria and ventricles, time from beginning of P  to beginning of QRS complex, usually 0.12 - 0.16 s.

QRS complex: depolarisation of ventricles, duration=  lead II is 0.08-0.12s  and 1mV not>35 mm

ST segment: is a straight line at end of ventricular depolarisation. From end of S wave to beginning of T wave. Here heart is depolarized, hence isoelectric, duration= 0.08s.

T wave: ventricular repolarisation, normally positive i.e. upwards, 0.16-0.27s and 0.2-0.3mV.

QT interval: time from the beginning of the QRS to the end of the T wave, 0.3-0.34s;

PR segment: time from end of P wave to beginning of QRS complex, 0.03-0.06s; impulse travelling through AV node, AV bundle and Purkinje fibres, no change in surface potential, hence isoelectric.

Heart rate = count the number of QRS complexes. Atrial repolarisation hidden by QRS complex.

Clinical Aspects: E.C.G. can be used to detect disturbances in initiation and propagation of action potentials (cardiac arrythmias), e.g. in Ischaemic Heart Disease. Another cause of disturbances would be generation of latent pacemakers (ectopic foci) along the conductive tree.The electrical axis gives the overall direction and size of the electrical impulses conducted over the heart, it is normally 59 degrees. It indicates the approx. position of heart in thoracic cavity and possible hypertrophy of heart chambers, i.e <0 degrees= left axis deviation, if >90 degrees= right axis deviation.

Arrythmias

Are heart rhythm abnormalities. There are 2 main causes, extra excitatory signals or malfunction of conductive system.

1.      Heart block: 3 types- i) 1st degree =incomplete heart block, very slow AVN conduction ii) 2nd degree = only a fraction of normal conduction iii) 3rd degree = no conduction between atria and ventricles eg. Ischaemic damage to AVN or bundle of His.  This may lead to new pacemakers (ectopic foci)  in purkinje or bundle of his.

2.      I) congenital conduction pathways eg. Extra pathway between atrial muscle and AVN thus Increase in heart rate to 150b/min-250b/min, problem caused by re-entry or recycling of impulse; there could also be a separate pathway between atria and ventricles causing again re-entry problems. II) Extra post depolarisations or extra depolarisations before repolarisation is complete due to increased Ca2+ current.

3.      Hypoxia- causes Ischaemia, which increases the K+ channels to open, thus shortens action potential and thus reduces contraction.

4.      Hyperkalaemia- increased K+ in plasma, causes cell membrane to depolarize, thus arrythmias and fibrillation

Treatments : ca2+ , K+ , Na+ channel blockers and beta blockers

Mechanical events of the cardiac cycle:                          

Figure (1) shows some of the mechanical events in one cardiac cycle for the left side of the heart. This includes the E.C.G., 2 heart sounds, pressure changes in the aorta and left ventricle and blood volume change in the left ventricle. 

One cardiac cycle is described below from one P wave to the next P wave.                                     

The P wave signals electrical excitation of the atria, spreads over atrial muscle, atrial contraction starts, thus slight increase in atrial pressures, and blood pumped into ventricles (0.16 s), excitation spreads over ventricles, QRS complex starts, ventricular contraction begins, thus increase in ventricular pressures, closes the atria-ventricular valves thus causing the first heart sound (Lubb), ventricles now become a closed chamber since the semilunar valves are already closed, ventricular pressures increase rapidly (isovolumetric contraction), exceeding the pressures in the pulmonary artery and aorta, thus opening the semi-lunar valves, ejection of blood from ventricles occurs (rapid phase followed by slower phase), ventricular relaxation (pressures drop, closing the aortic and pulmonary valves- thus 2nd heart sound- Dubb), at end of ventricular relaxation the atria ventricular valves open because ventricular pressures become less than atrial pressures, a phase of rapid filling of ventricles (0.1 s) followed by a phase of slow filling (0.2 s) occurs which is finally ended by the atrial systole.

Important features of the mechanical events:

Heart Sounds:

There are four heart sounds, two of which can be heard clearly on surface of chest with stethoscope. First is 'Lubb' has a f= 30-45 Hz,duration= 0.05 s, caused by AV valves closing and vibrations in cardiac muscle. Second is 'Dubb' occurs at end of T wave, with f= 50-70 Hz, duration= 0.025 s, caused by closure of semilunar valves. Abnormal heart sounds are called 'murmers', and can occur due to narrowing or increased resistance of pathways (e.g. valves) to blood circulation.                                                               

Aortic pressure wave:

Rising part is synonymous with pressure rise in ventricle. Highest pressure is the systolic pressure. Dicrotic notch is due to temporary backflow of blood from aorta into left ventricle, this backflow stops with closure of aortic valve, producing sharp recoil of walls of aorta, peripheral flow of blood continues due to elastic recoil of the arterial walls. Resting level is the diastolic pressure.

Left Ventricular Pressure Wave:- Shows 4 parts (1, 2, 3, 4)

Both rising(2) and falling parts(4) are the same shape. Rising part (Isovolumetric contraction) gives an indication of the strength of the heart, and determines systolic pressure and also the cardiac output. This is the most important waveform in terms of generating enough pressure and blood flow for the body. Notice the low starting and high finishing pressures of the waveform.

Left Ventricular Volume:

When the bicuspid valve is closed, the amount of blood accumulated in the left ventricle at the end of diastole is known as the End diastolic volume. When the semilunar valve is closed, the amount of blood left in the left ventricle is known as the End systolic volume.

Lecture 3. Blood Pressure:

Definition of blood pressure. Its importance and regulation. Short term regulation by hormones and baroreflex mechanism. Long term regulation by kidney and blood volume alterations. Measurement of blood pressure. Dysfunction: Hypertension and its importance to other diseases eg coronary heart disease, stroke.

Stephen Hales (1677-1761) - a clergyman, was the first to measure blood pressure in a horse. Claude Bernard (1813-1878) showed in 1851, that the sympathetic discharge to the blood vessels was excitatory (vasoconstrictor tone). Karl Ludwig (1816-1895) in 1847 invented the kymograph and made the first continous recording of blood pressure. Rene Laennec (1781-1826) invented the stethoscope.

In 1733, Stephen Hales (1677-1761, pastor, physiologist, botanist) connected a cannula or fine tube to a glass tube held vertically from the carotid artery of a mare, and found that the blood rose to 3m, and suggested connection between blood pressure and atmospheric pressure. This discovery had no effect on medicine for the next 150 yrs. He was also the first person to correctly measure the capacity of the LV, and to measure cardiac output per minute, the speed of the blood flow in the vessels. In 1876 Von Basch produced the first apparatus to measure blood pressure without cutting an artery, but it was complicated to use (despite modification by the Italian Riva-Rocci in 1896), but the principle was accepted, that of an inflatable tourniquet to which a manometer was attached. The method was refined by the russian surgeon Korotkoff in 1905, by applying stethoscope to pulse area.

Arterial blood pressure varies with age, sex, metabolic rate, emotional state, sleep, postural changes and other factors. Normal values are expressed as a range. e.g. age 20-24, male systolic= 105-140, female systolic=100-130, male diastolic= 62-88, female diastolic=60-85. Arterial blood pressure increases with age, with pressures of women being 5-10 mmHg lower on average until the age of 50, after which pressures don't differ. An individuals blood pressure is normally expressed as systolic/diastolic. Hypertension is quoted as 165/95 and above. Moderate hypertension is 140/95.

Maintanance of an adequate blood supply to the brain, heart and kidney is intimately dependant on the level of the general arterial pressure (mean arterial pressure- M.A.P.). The M.A.P. is the average pressure during the cardiac cycle. M.A.P. is also equal to = Diastolic pressure + 1/3(pulse pressure)

	M.A.P. = C.O. x T.P.R.

 

The M.A.P. is the result of discharge of volume of blood from the heart to the arterial system, which cannot all escape through to the venous system before the next beat occurs. This means i) the arterial system is overfilled and ii) elastic arterial walls are stretched. Thus M.A.P is dependant on the cardiac output (C.O.) and the total peripheral resistance (T.P.R.). Thus factors affecting C.O. (the output of blood from the left side of the heart) and T.P.R. (the total resistance offered by the vessels to blood flow) will determine the value of M.A.P.

The systolic ejection of blood from the left ventricle to the aorta, creates a pressure waveform (arterial pulse wave) in the aorta and is transmitted to the rest of the arterial tree (refer to the aortic pressure waveform on handout). This waveform is asymmetrical. The peak of this waveform is the systolic pressure (120 mmHg) and the base (when heart is relaxing) is the diastolic pressure (80 mmHg). M.A.P.(approx. 100 mmHg) is the average effective pressure forcing blood through the circulatory system and is midway between these two pressures. Arterial pressure is pulsatile during each cardiac cycle. The pulse pressure which can be felt readily on the radial and carotid arteries, is the difference between the systolic and diastolic pressures. The blood pressure within an artery varies during each cardiac cycle and hence the arterial pulse wave varies. The size and shape of the arterial pulse wave are directly related to the stroke volume and inversely related to the compliance (elasticity) of the arterial vessels. The speed of this wave is slow in the large arteries (3-5m/s)

and faster in the small arteries (14-15m/s) and this also relates to elasticity.

Factors affecting blood pressure:

1/ C.O. = stroke volume x heart rate

2/ Starling effect- increased stretching of heart muscle leads to increased contraction.

3/ Sympathetic stimulation- causes an increase in heart rate, and in force of contraction.

4/ Parasympathetic stimulation- mainly decreases the heart rate and slight decrease in force.

5/ Peripheral resistance- particularly of the arterioles. Sympathetic nerves are extremely important in regulating blood pressure and thus blood flow.If these arteriole vessels constrict, then the outflow to the veins is temporarily reduced and thus M.A.P. is increased, whilst if vessels dilate, M.A.P. is decreased. Variations in the diameter of the arterioles of the abdominal (splanchnic) region are more effective than other areas in causing changes in M.A.P. The splanchnic vessels when fully dilated have an immense capacity to hold blood volume. Sudden strong emotion may cause their dilation, and thus a fall in M.A.P. and may lead to fainting.

6/ Blood volume- a sufficient amount is required to overfill the arterial system. Haemorrhage causes a decrease in blood volume and thus M.A.P. falls. Atrial Natriuretic Peptide (ANP or ANF), released from the atria due to stretching of atria, can decrease blood volume in minutes, by action on the kidney to increase water loss, decrease sodium reabsorption, and also decrease release of ADH and renin/aldosterone. It also causes vasodilation of arteries and veins. Blood volume can be increased by the hormones renin, angiotensin II, aldosterone and ADH, which can thus raise blood pressure.

7/ Viscosity- Blood is 5 times more viscous than water. Thus increased viscosity causes an increase in resistance to blood flow and thus increased work for the heart.

8/ Elasticity of the arterial walls- elasticity (and thus the recoil of the vessel walls) and the peripheral resistance ( to prevent escape of too much blood to the venous system) are essential for the development of the diastolic pressure.

Control of blood pressure:

This can be split into short term (minutes, hours- e.gs posture, acute stresses, haemorrhage) to long term (days, weeks- e.gs blood volume, hypertension).

Short Term control:

Baroreceptor reflex: (negative feedback control).

This reflex maintains short term control 60% of the time. High pressure receptors called arterial Baroreceptors (nerve endings in vessel walls) are found in the arch of the aorta and the carotid sinus, and they respond to stretch. They monitor the pressure of the blood comming from the aorta and carotid artery respectively. They have two reflexes affecting the heart and thus cardiac output and the blood vessels and thus the peripheral resistance.

Consider a rise in blood pressure in the body:

This will cause an increased discharge from the baroreceptors via the vagus and glossopharyngeal nerves to the cardivascular control centres (cardiac and vasomotor area in the medulla- excitatory and inhibitory areas) in the brain. This leads to an increased discharge of parasympathetic nerves to the heart and a decreased discharge of the sympathetic nerves to the heart, with the effect of decreasing the heart rate and stroke volume. There is also a decreased discharge down the sympathetic nerves to the arterioles, producing vasodilation and thus a decrease in peripheral resistance and the net overall effect is to return blood pressure to normal. The reverse of these changes take place for a fall in blood pressure in the body.

Certain situations the baroreflex may be suspended temporarily, e.gs. i) during exercise- increase in systolic pressure during exercise ii) diving (face immersion) reflex- sharp decrease in both heart rate and arterial pressure iii) stress- increase in blood pressure.

Cardiopulmonary reflexes:

There are a variety of other receptors which sense low pressures, mainly in the walls of the heart (atria, ventricles), pulmonary vessels and vena cava which supplement and modulate the baroreceptor reflexes. These receptors are mainly affected by stretch. The resulting reflexes are involved in both short term and long term control. e.g. increased stretch of the atrium, releases ANF, which affects the kidney to alter the blood volume. A decrease in atrial receptor stimulation can increase blood volume. Both inhibitory (e.g. bradycardia, vasodilation and inhibition of breathing) and excitatory responses can be produced from receptors in the ventricles mediated by vagal and sympathetic nerves and local metabolites (e.g. prostaglandins, serotonin, bradykinin).

Long term control: Involves regulation of the normal blood volume of 5.5 litres. This means regulation of the plasma volume (PV) and the red cell volume (RCV). RCV is determined by the number of red blood cells, thus bone marrow and erythropoietin and changes take place more slowly in days and weeks. PV is affected by both fluid input and fluid loss and thus more rapid changes. The main factor in regulation is the kidney, which regulates the water and sodium content. Sodium is extremely important to maintaining the plasma volume. Factors which affect the blood volume include:

i) Vasopressin (ADH)- released from the posterior pituitary and decreases water loss and thus sodium reabsorption ii) Renin-angiotensin-aldosterone system - If renal arterial pressure is low, or low sodium chloride, or increased renal sympathetic activity leads to secretion of the hormone renin, which breaks the plasma protein angiotensinogen into angiotensin I and then angiotensin II. The latter is a powerful vasoconstrictor (half life 30s), and also increases sodium reabsorption by proximal tubule, and stimulates the release of aldosterone (and cortisol) from adrenal cortex, which reabsorbs sodium and also stimulates ADH release. iii)Atrial Natriuretic Peptide (ANP)- Is a 28 amino acid released from the atria by large atrial stretch, which produces diuretic responses from kidney, also vasodilation and decrease in renin release. IV) Renal efferent nerves (sympathetic fibres)- increased activity leads to direct sodium reabsorption by proximal tubule and activation of ii)  and thus increase in plasma volume. v) Factors which affect venous capacitance can affect distribution of blood within the body.

A variety of drugs are used to decrease high blood pressure (hypertension). These drugs bring about their effects by i) vasodilation - e.g. Hydralazine ii) Smooth muscle tension decrease calcium channel blockers e.g. Nifedipine iii) changing blood volume - diuretics e.g Thiazides iv) Angiotensin Converting enzyme inhibitor- e.g. Captopril v) reducing the cardiac output of the heart - reducing the sympathetic effects on the heart e.g. Propranolol

Measurement of Blood Pressure:

A direct invasive measure can be obtained from radial artery puncture and connecting needle and catheter to a pressure transducer. Riva Rocci first suggested an indirect measure of blood pressure. The most common non-invasive procedure is the method of Auscultation (sounds) developed by a Russian surgeon called Korotkoff in 1905. The apparatus involves a Stethoscope to listen to sounds and a sphygmomanometer consisting of an inflatable cuff (Riva-Rocci), a mercury manometer to measure pressure, a small rubber handpump with valve to increase or decrease pressure. Subjects sit on a comfortable chair with either their left or right arm resting on a flat surface. After removal of any restraining clothes, a cuff of appropriate size is wrapped around the upper arm. The cuff is inflated to a pressure of 150-160 mmHg. After placing the stethoscope drum on the Brachial artery, the pressure in the cuff is released gradually, after a while sounds can be heard (Korotkoff sounds) until the first heart sound is heard (this is the systolic pressure), pressure drop is allowed to continue when further sounds can be heard. The dissapearance of the last sound determines the diastolic pressure.

Demands on the Cardiovascular System

AIMS

1. Exercise, Stress, shock

2. CHD and Hypertension?

3. Treatments for CVD?

EXERCISE

• Definition: A single bout of bodily exertion or muscular activity that requires energy expenditure above resting level, resulting usually in voluntary movement.
• Description: Intensity (maximal or submaximal);duration; type
• Aerobic (dynamic, isotonic)
• Non-aerobic ( isometric, static) Isokinetic

Successful  exercise

•          muscular, CVS, respiratory

•          Adequate gas exchange- O₂ & CO₂

•          Availability of fuel- glycogen, glucose, fatty acids

STEPS IN EXERCISE

    3 STAGES

• 1. Anticipation- preparatory, HR,  C.O.
• 2. During- main changes- metabolic, respiratory,CVS, blood flow redistribution
• 3. Recovery- return to resting conditions, payback of O₂ debt, metabolic replenishment

Physiological changes

CVS

INCREASE:

•          blood flow to muscles

•           1 to 22-33 l.min^-1

•           SNS, A, NA

•           metabolic hyperaemia

•           indirect PNS

 

-          SP, DP, C.O. SV, HR 

                                              

 

•   Respiratory

–        V_E, Pulmonary blood flow, bronchial dilation, VO₂

–        O₂ , CO₂, anaerobic metabolism, pH, RQ

–        O₂ extraction- intensity, capillary density, Bohr shift to right, aerobic enzyme activity

Limitations to exercise

• Healthy

–        gas exchange-delivery/extraction of O2,removal of CO2; maximal cardiac output

–        availability of fuel/metabolic capacity of active muscle

–        controlling body core temperature

–        muscle fatigue

–        increase in lactate

• Disease
• Jones & Killian (2000). Exercise limitations in health and disease- NEJM 343(9):632-641

–        Pain, dyspnoea, increase in perceived effort

–        reduced aerobic and ventilatory capacities

–        muscle weakness

What is shock?

‘Acute circulatory failure

-general cellular hypoxia

 -inadequate tissue perfusion’

CAUSES?

• Inadequate blood flow to vital organs 

Cells unable to use O₂

Symptoms

• low C.O.
•  low B.P.
•  pale, grey
•  rapid shallow breathing
•  rapid weak pulse
•  decreased urine

Types  of  shock?

w  Hypovolaemic

w   Cardiogenic

w   Mechanical

w   Septic

w   Anaphylactic

Cardiovascular Disease

• CAD [ CHD, IHD, ]

–        Ischaemia, atherosclerosis, arrythmias, thrombosis, angina, MI,

–        major cause of death in western world

–        Hypertension, Heart failure, Valve disease, cardiomyopathies, congenital, Tachyarrythmias and Bradyarrythmias, cardiac infections, pulmonary embolism, MI, Hyperlipidaemia, aortic dissection,CHD

PRIMARY RISK FACTORS

• SMOKING

–        4000 chemicals- diseases of lungs, heart, blood vessels, cancer

–        risk µ no. Of cigarettes

–        Nicotine- addictive, increased A + NA,  fatty acids, stickiness of platelets, decrease  fibrinolysis

–        CO- carbamino compounds, decreases ability of Hb to transport O2, arrythmias

• HYPERLIPIDAEMIAS

–        lipids- fatty acids, cholesterol, lipoproteins, chylomicrons, triglycerides

–        increased by diet, diabetes, ideopathic

–        risk  µ [cholesterol]; risk µ LDL; risk µ 1/HDL

–        risk µ 1/ fish oils (w3, w6- FFA)

• HYPERTENSION

–        increase in SP, DP, TPR - increased workload

–        increase in blood volume e.g Na+

MECHANISMS

• Atherogenesis- plaque formation-(fatty streak, fibrous plaque, complex lesion)
• plaque= lipid rich core surrounded by fibrous cap, stable or unstable
• LIPIDS- increased amt deposited on intimal layer- complex plaques
• SMOOTH MUSCLE- no. Increased, secrete collagen and elastin to form complex plaques
• ENDOTHELIUM  DYSFUNCTION

–        vascular tone

•          thromboxane A2, endothelin,

•          prostacyclin, NO

–        stickiness of lining

–        clot formation -increased fibrinogen

–        uptake of inflammatory cells

–        endothelial damage- free radicals

–        uptake of LDL and oxidized LDL

• complex plaques or ruptured  plaques occlude lumen- angina, arrythmias, sudden death

HYPERTENSION

• 1 in 10 adults- high blood pressure
• 140/90, 160/95
• Age (>45)
• Gender (M>F)
• Major health problem

–        Strokes, heart failure,

–        Major risk factor- chd, dm

–        Renal failure, tpr, lv  hypertrophy

–        risk µ pressure

• Basic cause unknown

–        2 types

–        Essential- 90-95%

–        Secondary- 5-10%

CAUSES

• kidney disease- renal artery stenosis
• obesity, alcohol, cushing’s syndrome, aldosteronism
• MAP= C.O. X T.P.R
• VASOCONSTRICTOR AGENTS

–        ANS- increased SNS activity

–        A, NA, angiotensin II, ADH, 5HT, PROSTAGLANDINS

• VASODILATOR AGENTS

–        KININS, NO, ENDOTHELIAL DAMAGE, Ach

• IONIC IMBALANCE

–        Na+, K+, Ca2+

• OBESITY

–        BMI, WAIST/HIP RATIO

–        INCREASED SV, C.O., SNS, PLASMA VOLUME, INSULIN, RENIN/ALDOSTERONE

•  ALCOHOL

–        increased  pressor effect, SNS, cortisol, renin/angiotensin, sensitivity  to adrenaline

• INSULIN  RESISTANCE- DIABETES

–        increased  Na+, Ca2+, SNS

• family history, genetic, environment
• MISDIAGNOSIS

TREATMENTS

• AIMS

–        Pain, O₂ demand, workload

–        Quality of life, mortality risk

• DRUGS

–        NITRATES, b- BLOCKERS, Ca²+ antagonists, anticoagulents, lipid lowering

• SURGICAL

–        CABG, PTCA, Revascularisation, left ventricular assist devices, heart transplants

• LIFESTYLE CHANGES

–        Diet, weight control, exercise, stop smoking

DRUGS

• Nitrates- GTN, Isosorbide dinitrate

–        relieves angina in minutes

–        vasodilator- veins, arteries, coronary vasospasm, thrombosis, platelet aggregation

–        side effects- headaches, B.P, HR

• Ca²+ antagonists- Nifedipine, Verapamil

–        relieves angina - vasodilation of blood vessels

–        block ca2+ channels- smooth muscle> cardiac

–        side effects- headache, BP, peripheral oedema, AV node conduction block,  force

• b- blockers- Propranolol

–        decreases O₂ demand, HR, SV

–        side effects- -ve inotropy, C.O

• Anticoagulents- Aspirin, Heparin, LMW heparins, Hirudin,streptokinase, warfarin

–        decreases clotting- suppresses platelet aggregation

–        inhibits thrombin, clotting factors, increases prostacyclin, inhibits platelet receptors

• Analgesics- diamorphine, diuretics- thiazides, ACE inhibitors- Captopril,  a-blockers- hydrallazine,
•  lipid lowering- statins (simvastatin, fluvastatin), Niacin ( nicotinic acid),  Resins (colestipol)

–        decrease LDL, triglycerides, increase HDL

–        decrease lipoprotein synthesis in liver

SURGICAL

• PTCA= percutaneous transcoronary angioplasty

–        less invasive, faster recovery, cheaper, quick relief from symptoms

–        risk of clot being dislodged, ischaemia, restenosis, long term improvement poor, metal stents

• CABG = coronary artery bypass grafting

•          vessels >70%  stenosis- require grafts

•          long saphenous vein, leg, 15cm  needed, occlusion

•          Internal mammary atery, chest, high reliability, long term usage, low occlusion rate

–        Operation

•          monitor ECG, T, Blood, K+, clotting times

•          patient anaesthetized, heparinised, chest exposed, heart connected to  bypass machine, core temp= 26-28C

•          to operate heart needs to be still (infuse cardioplegic solution), have little blood (clamping aorta)

–        Disadvantages

•          invasive, expensive, bleeding, poor cardiac output, arrythmias, post infection

–        Advantages

•          80% of patients have complete relief, long term survival >10yrs

RESOURCES
Websites
 Cardiovascular physiology online
 Body fluids - somewhat good
 Interactive Physiology Pearson

more resources will be added