Physiotherapy Management Cardiorespiratory 1 lecturenotes lectures 1to8 2019 2020 PDF

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Physiotherapy Management Cardiorespiratory 1Lecture notes of academic year 2019-Lecture 1: Haemodynamics: Pressure, Flow and ResistanceLecture objectives: ▪ Understand the driving force behind blood flow.▪ Define the laws of resistance.▪ Know the three types of blood flow, which occurs in each vesse...

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Physiotherapy Management Cardiorespiratory 1 Lecture notes of academic year 2019-2020

Lecture 1: Haemodynamics: Pressure, Flow and Resistance Lecture objectives: ▪ Understand the driving force behind blood flow. ▪

Define the laws of resistance.

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Know the three types of blood flow, which occurs in each vessel type and why.

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Understand the terms compliance and tension and how these are calculated.

Blood Flow A pressure gradient drives blood flow; blood flows from an area of higher pressure (the aorta) to an area of lower pressure the (venae cavae). While blood flows through the systemic circulation it is all the time decreasing in pressure. ▪ ▪ ▪

Aortic pressure ~90mmHg. Vena cava pressure (close to right atrium) ~0mmHg. This creates a pressure gradient ∆P, which is effectively equal to the mean arterial pressure (MAP): the average blood pressure in an individual, it is the average arterial pressure during a single cardiac cycle.

Darcy’s Law Darcy’s law: flow is linearly proportional to the pressure difference between two points. Darcy’s law is a simple mathematical statement that neatly summarises the following: ▪ if there is no pressure gradient over a distance, no flow occurs (these are hydrostatic conditions), ▪ if there is a pressure gradient, flow will occur from high pressure towards low pressure (opposite the direction of increasing gradient - hence the negative sign in Darcy's law),

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the greater the pressure gradient (through the same formation material), the greater the discharge rate, and the discharge rate of fluid will often be different – through different formation materials (or even through the same material, in a different direction) – even if the same pressure gradient exists in both cases.

󰇗 𝑃1 − 𝑃2 𝑄󰇗 = 𝐾(𝑃1 − 𝑃2 ) = 𝑅 Where: – Q = fluid flow rate (m3.s-1) – K = some constant – P1 = pressure at point 1 (Pa) – P2 = pressure at point 2 (Pa) – R = resistance to flow ▪ ▪ ▪ ▪

Darcy’s law concerns fluid flow (volume/time). This is not the same as fluid velocity (distance/time). Mean velocity = flow/total cross-sectional area. As total cross-sectional area increases mean velocity falls. Total flow is not altered: it remains equal to the cardiac output at each level of the vascular system.

Poiseuille’s Law Poiseuille’s law: a physical law that gives the pressure drop in a fluid flowing through a long cylindrical pipe. Blood flow is met with resistance as it flows around the body. This resistance to flow can be in the form of: ▪ vessel radius (r) ▪ fluid viscosity (η) ▪ vessel length (L)

𝑅= Where: – R = resistance – η = fluid viscosity – L = vessel length (m)

8𝜂. 𝐿 𝜋. 𝑟 4

– r = vessel radius (m) So, if we combine Darcy’s and Poiseuille’s laws we get Darceuille…

󰇗 𝜋. 𝑟 4 𝑄 = (𝑃1 − 𝑃2 ) × 8𝜂. 𝐿 ▪ ▪ ▪

Flow is extremely sensitive to vessel radius. A fall in radius from 1 cm to 0.01cm will increase resistance by a factor of 108. This is why the arterioles are the main site of resistance.

Total Mechanical Energy of Fluid Houston, we have a problem… The MAP in the aorta is around 95mmHg and the MAP in the arteries of the foot is around 180mmHg. These values mean that in a standing person, Darcy’s law would predict that blood would flow from the foot to the aorta through the arteries! Obviously, this does not happen, but why not? Bernoulli has the answer! Why are they all French? Bernoulli’s Theory Pressure energy = pressure x volume (PV), P Potential energy = fluid mass (density,  x volume, v),  x height, h x gravitational force, g. This is equal to vhg. Kinetic energy is dependent on fluid mass (v),  and velocity (). This is equal to v2/2.

𝜌𝜈 2 𝑀𝑒𝑐ℎ𝑎𝑛𝑖𝑐𝑎𝑙 𝑒𝑛𝑒𝑟𝑔𝑦 = 𝑃 + 𝜌𝑔ℎ + 2 Mechanical energy is measured per unit of volume. Bernoulli’s theory can be used to solve the problem described earlier… The problem was that the MAP in the aorta is 95mmHg but the MAP in the arteries of the foot is double that at a whopping 180mmHg. This means blood should flow from the foot to the heart through the arteries but obviously what is observed is the other way round.

The reason why it is the other way round is that blood in the aorta has around 90mmHg potential energy. If this is added to the MAP of blood in the aorta, the total pressure is around 185mmHg. 185mmHg is just greater than the 180mmHg observed in the arteries of the feet (which I’m assuming we’re assuming and Bernoulli’s assuming has zero potential energy) and this difference is enough to drive blood flow (in the correct direction). Series and Parallel Circuits Vessels are arranged in series (end to end) and in parallel (branched) with other vessels. ▪ Total resistance increases if series units are added. Recall for AS Physics that resistance in series is simply equal to the sum of each individual component in the circuit, so the resistance just gets bigger. ▪ Total resistance decreases if parallel units are added. Again, from AS Physics the resistance in parallel is equal to the inverse sum of each individual component in the circuit, so the resistance gets smaller.

Flow in Blood Vessels Three different patterns of flow occur in the circulation: 1. Laminar flow: this occurs in normal arteries and veins. 2. Turbulent flow: this occurs in the ventricles and sometimes in the aorta. 3. Single-file flow: this occurs in the capillaries. Laminar flow The liquid behaves like a series of thin concentric cells (the laminae) sliding past each other. The lamina in contact with the vessel wall is held stationary by molecular cohesive forces (i.e. it has no velocity). The adjacent lamina slides slowly past each other gaining velocity. Maximum velocity is reached at the centre of the tube; the ones in the middle are getting one hell of a ride! An atheromatous plaque can lead to turbulent flow once the blood has flown past the plaque. Turbulent flow If the pressure gradient increases, flow will increase linearly. A point is reached when flow increases only in proportion to the square root of the pressure; this is due to turbulence. In turbulent flow, some pressure energy is dissipated as heat. Turbulent flow is encouraged by: ▪ high fluid velocity (). ▪ large tube diameter (D).

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high fluid density ().

Turbulent flow is discouraged by: ▪ high fluid viscosity (η) These above factors are combined to give the Reynold’s number:

𝑅𝑒 =

(𝜐. 𝐷. 𝜌) 𝜂

Reynold’s number: is a dimensionless quantity that is used to help predict similar flow patterns in different fluid flow situations. It is defined to be the ratio of inertial forces to viscous forces and consequently quantifies the relative importance of these two types of forces for given flow conditions (Falkovich, G. (2011) Fluid Mechanics).

Single-file flow The diameter in capillaries is around 6-10μm, with the diameter of a red blood cell being around 8μm. Red blood cells are forced to continue in single file and to deform into parachute-esque configuration (the red blood cells’ biconcave shape allows them to basically fold). Laminar flow in the capillaries is impossible as plasma is trapped between the red blood cells. This single-file flow is affected in conditions such as sickle-cell anaemia: red blood cells that assume an abnormal, rigid sickle shape. Compliance Compliance: the ability of a hollow organ (vessel) to distend and increase volume with increasing transmural pressure or the tendency of a hollow organ to resist recoil towards its original dimensions on application of a distending or compressing force. It is the reciprocal of ‘elastance’, hence elastance: a measure of the tendency of a hollow organ to recoil toward its original dimensions upon removal of a distending or compressing force. Transmural pressure: the difference in the pressure of inside and outside the vessel. Compliance, in mathematical terms, is the change in volume per unit change in pressure.

𝐶𝑜𝑚𝑝𝑙𝑖𝑎𝑛𝑐𝑒 =

Δ𝑉 Δ𝑃

Where: – ΔV = change in volume. – ΔP = change in pressure. Compliance in arteries and veins Veins have thin walls and are easily stretched; this means they are described as possessing a higher compliance (or ‘capacitance’) than arteries. Veins can accommodate large increases in blood volume in response to a small increase in blood pressure. ▪ ▪

Veins are volume reservoirs. Arteries are pressure reservoirs.

Forces in the blood vessel wall The distending pressure stretches the vessel wall. Unless this force is balanced by forces within the vessel wall (tension, T) the vessel will rupture. The magnitude of tension in the wall necessary to withstand the transmural pressure (Pt) is influenced by both the vessel radius (r) and the wall thickness (μ). This relationship is expressed by the Law of LaPlace:

𝑇=

𝑃𝑡 𝑟 𝜇

Where: – T = tension – Pt = transmural pressure – r = vessel radius – μ = vessel wall thickness In large arteries, the transmural pressure and radius are large, so the wall needs to be thick in order to compensate. In capillaries, the transmural pressure is quite low and the radius is very small; this allows the walls to be very thin. The likelihood of vessel rupture is greatest in elastic arteries: rupture of the aorta is a relatively common (and usually fatal) medical event. It’s a chat show Jim, but not as we know it.

Lecture 2: The Microcirculation and Lymphatic System Lecture objectives: ▪ The microcirculation. ▪

Local regulation of blood flow.

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Transcapillary solute exchange.

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Starling’s forces.

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The lymphatic system.

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Oedema.

The Microcirculation ▪ ▪ ▪

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The microcirculation is the circulation of blood through the smallest vessels – the smallest arterioles, the capillaries and the smallest venules. Capillaries form a network called a ‘bed’ referred to as a ‘capillary bed ’. The capillary bed is the place of solute exchange and comprises of three things: 1. The ‘true’ capillaries themselves; where the solute exchange takes place. 2. The metarterioles; the vascular shunt that provides a bypass pathway through the capillary bed. 3. The precapillary sphincters; these relax or constrict to regulate blood flow through the capillaries. Density is highest in metabolically active tissues with the capillary bed being so dense it actually forms more of a ‘sheet’ than a ‘matrix’, surrounding the organ. The more metabolically active tissues obviously require an extremely efficient solute exchange; the more active the tissue, the more dense the capillary bed. Flow depends upon the contractile state of the smooth muscle in arterioles.

Local Regulation of Blood Flow Autoregulation is the intrinsic adjustment of blood flow to a tissue so flow meets tissue requirements. Regulation is not dependent on extrinsic factors such as the autonomic nervous system. For example: metarterioles themselves can sense the

requirements of the tissues it is supplying and therefore can automatically adjust their contractile state accordingly. Because the vessels themselves initiate the regulation, it is known as intrinsic autoregulation. Metarteriole: a short vessel that links arterioles and venules. Instead of a continuous tunica media, they have individual smooth muscle cells placed a short distance apart, each forming a precapillary sphincter that encircles the entrance to that capillary bed. Changes in local blood flow are controlled by two main mechanisms: 1. Changing arteriole diameter: increase blood flow through, dilation and more blood flows through capillary bed. Vasodilation. 2. Altering the degree of contraction of the precapillary sphincters: by contracting it will cut off the blood flow through that vessel. How does the metarterioles know there is an increased demand? These intrinsic control mechanisms may be classed as either metabolic or myogenic.

Metabolic Control ▪

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As the rate of metabolism increases, the perfusion rate to that particular tissue increases. This makes logical sense – a more highly active tissue has a higher demand for the supply of O2 etc. and the removal of waste products. This relationship still exists despite no changes to perfusion pressure (perfusion pressure remains constant) and no changes from the autonomic nervous system. Therefore there must be a mechanism within the vessels themselves to adjust accordingly. Therefore it is characterised as an intrinsic property of the microcirculation.

O2 as a factor in metabolic autoregulation As the metabolic rate increases, blood flow increases. How do the vessels know metabolism has increased? When the tissues are highly active they will consume a lot of O2, because they need more ATP to be produced, so their demand for O2 increases. At this stage there is no increase in blood flow. If the high demand cannot be met, there would be a decrease in oxygenation of the tissues; in the area surrounding the tissues, hypoxia would occur. This hypoxia can be detected by the smooth muscle in the arterioles surrounding the active tissues. The smooth muscle cells in the tunica media detect this hypoxia and in response they relax, dilating the vessel, increasing diameter, decreasing resistance, therefore increasing blood flow and increasing O2 supply. Negative feedback prevents the cycle from prolonging. Waste products as a factor of metabolic autoregulation

Tissues that are more active are producing more waste products e.g. CO2, H+, K+ and adenosine. These waste products accumulate in the tissues surrounding the vessels and can diffuse to the location of the vessels. When this occurs, these waste products too trigger the relaxation of smooth muscle in the tunica media. Dilation of the vessel results, increasing diameter, decreasing resistance, therefore increasing blood flow and increasing O2 supply. This is needed to expel the waste products also. Other factors involved in metabolic autoregulation In response to increased pressure, increased synthesis of waste products and/or tissue hypoxia, the endothelium (tunica intima) of the vessels itself produces vasodilating agents such as prostacyclin and NO, which diffuse to the tunica media to cause the relaxation of smooth muscle. As before, dilation of the vessel results, increasing diameter, decreasing resistance, therefore increasing blood flow and increasing O2 supply. This is needed to expel the waste products also. Originally known as endothelium-derived relaxing factor, NO is produced in endothelial cells (of the tunica intima) by the enzyme nitric oxide synthase in response to the above factors along with, as the picture suggests, shear stress. Larginine is reacted with NADPH, H+ and O2 to form citrulline, NO and NADP+: L-arginine + 3/2 NADPH + H+ + 2O2 ⇌ citrulline + nitric oxide + 3/2 NADP+ NO then acts through the stimulation of the soluble guanylate cyclase, the enzyme responsible for the subsequent formation of cGMP. cGMP activates protein kinase G, which causes reuptake of Ca2+ and the opening of Ca2+-activated K+ channels. The fall in concentration of Ca 2+ ensures that the myosin light-chain kinase can no longer phosphorylate the myosin molecule, thereby stopping the cross-bridge cycle and leading to relaxation of the smooth muscle cell. This discovery allowed the mode of action of drugs e.g. glyceryl trinitrate (GTN) to be understood – it works as a NO donor, hence acts as a vasodilator. Myogenic Control Myogenic control is achieved by muscles (myo, muscle). Despite pressure increases as blood flows around the systemic circulation, the rate of blood flow through a vascular bed is kept constant over a wide range of perfusion pressures. This is important, as it is undesirable for the capillary blood flow to increase uncontrollably, just because there has been an increase in systemic circulation pressure. Flow through the capillary bed must only be related to the needs of the tissue, nothing else.

Darcy’s law states that an increase in pressure leads to an increase in blood flow, but as can be seen from the graph, this doesn ’t occur over a physiological pressure range. There must be mechanisms in place that are contributing to this maintenance of blood flow through the capillaries despite an increase in pressure. Darcy’s law states that flow = (pressure gradient/resistance). ▪ Pressure stays the same then flow will stay the same. ▪ An increase in pressure means an increase in blood flow but as can be seen this is not the case. An increase in resistance must be matching the increase in pressure, balancing it out so no increase in blood flow is observed. This increase in resistance is initiated via contraction of the smooth muscles cells.

How does this happen in terms of its myogenic mechanisms? Mechanism of the myogenic response No metabolic agent is triggering vasoconstriction; it is the smooth muscle itself that is responsible. When an increase in perfusion pressure is detected, the vessels begin to stretch. This stretch is telling the vessel that perfusion pressure has increased. Since an increase in flow isn ’t desirable, this stretch is the stimulus to activate vasoconstriction. An increase in pressure doesn’t cause an increase in blood flow because: when the increase in pressure is sensed by the vessels, they naturally stretch (accommodation) and it is this stretch that is the stimulus for the vessels to narrow. The increase in pressure is counteracted by an increase in resistance caused by vasoconstriction and systemic perfusion through the capillary beds remains constant. Negative feedback prevents the prolonging of the cycle. All the examples described above are short-term and extremely localised mechanisms to counter increased perfusion pressure. Long-term Autoregulation If the nutritional or O2 demands of a tissue chronically exceed delivery, long-term autoregulation develops over a period of weeks/months. Long-term autoregulation occurs in two ways: 1. An increase in the number of microcirculatory vessels supplying the tissue. If the muscle increases in size and average activity, capillary bed density increases (angiogenesis) to meet the new demands placed upon it.

2. Enlargement of existing vessels. This allows a greater surface area for solute exchange to take place. Examples of when the two above may occur: ▪ the partial occlusion of a coronary vessel. ▪ chronic exposure to high altitude (i.e. to a low Po2).

Transcapillary Solute Exchange Lipophilic solutes (e.g. O2 and CO2) enter and leave the capillary via the transcellular route. They are capable of diffusing in and out of the cell from the interstitial space through the plasma membrane (as they are lipophilic) and don ’t need a protein carrier or transport mechanism to do this. Hydrophilic substances cannot pass through the plasma membrane so do not travel in and out of cells via the transcellular route; instead they take the intercellular route. Hydrophilic solutes cross through the intercellular route via intercellular clefts, which have a diameter of around 60Å (60x10-10m). Intercellular clefts can be easily traversed by water, ions and other small hydrophilic organic solutes but proteins such as albumin and other plasma proteins cannot cross, as they have a diameter of around 70Å (70x10 -10m): they are too large so remain in the capillary! Just focusing on continuous capillaries. The fenestrated capillaries differ only really in the fact they allow the exchange of larger solutes (because of the larger gaps present). Exchange of Fluid between Capillaries and Tissues The distribution of fluid between the plasma and the interstitial fluid is in a state of dynamic equilibrium; fluid is constantly moving between the capillaries and the interstitial fluid: all the fluid surrounding the tissues where the capillaries are supplying the tissue with nutrients. The solutes are being exchanged from within to o...