Karteikarten
Module 2.06 physiology
Karten in diesem Stapel (95)
- 1Pulse PressureThe difference between systolic and diastolic pressure
- 2MAPMean Arterial Pressure -
diastolic BP + 1/3 Pulse Pressure
Because the heart is in diastole 60% of the time - 3Arteriole Pressure65mmHg
- 4Capillary PressureArteriole end - 20mmHg
Venule end - 15mmHg - 5CVPCentral venous pressure - is the venous pressure at the level of the heart (0mmHg)
- 6Function of the Cardiovascular system (5) Modulation of function1. Transport of O2, glucose and nutrients to tissue
2. Transport of CO2 and waste products to excretory organs
3. Transport of hormones
4. Transport of immune components
5. Thermoregulation
Modulated by the ANS - 7COCO = SV * HR
- 8Chordae Tendinae/TrabeculaeAV valves are prevented from being everted into the atria by high pressure in the ventricle by fine cords which are attached to each cusp on one end and the papillary muscle on the ventricles
- 9Valves - inorder of flow1. Tricuspid
2. Pulmonary
3. Mitral
4. Aortic - 10Stenosis of the valvesNarrowed valves - impari ventricular filling and increase afterload
- 11Regurgitiation of valvesIncompetent val;ves do not close properly
- 12SAN - LocationClose to the coronary sinus in the right atrium
- 13Spontaneous depolarisation of the SAN (3)1. Resting potential is -60mV
2. Decays steadily until -40mV due to the slowly reducing outward K+ current
3. Upstroke of AP is lsow and ONLY due to L-type Ca2+ channels - NO fast volatge-gated Na+ channels - 14Pacemaker potentialRate of decay of the SAN resting potential determines the time taken to reach the threshold and generate another AP - this determines heartbeat
- 15ChronotropesAffect the HR
Postive chronotropes (increase rate of decay): Noradrenaline
Negative chronotrope (decreases rate of decay): Acetylcholine - 16Conduction of AP through atriumAP activates adjacent atrial myocytes via gap junctions contained in intercalated disca - desomosomes provide the physical link
- 17What prevents the AP from reaching the ventriclesAnnulus fibrosus
- 18Annulus FibrosusIs a fibrous band of connective tissue which separates the atria and the ventricles.
1. Prevents electrical conduction between the atria and the ventricles - except at the AVN
2. Provides skeleton for the attachment of muscle and valves - 19Properties of the endocardium/endotheliumAnti-thrombogenic surface
- 20Function of the pericardium (2)The pericardium is a fibrous sheath that contains interstitial fluid
1. Prevents damage from friction
2. Prevents excessive enlargement of the heart - 21Pulmonary Artery Pressure20/15mmHg
- 22Location of the AVNBetween the RA and RV near the atrial septum
- 23Function of conduction delay in the AVNDelay of 120ms - allows atria to fully contract and complete ventricular filling
- 24Ventricle muscle contraction (7)1. Resting Potential is -90mV
2. Threshold for depolarisation is -65mV
3. Fast voltage-gated Na+ channels activate
4. Inward movement of Na+ (depolarisation to +30mV)
5. Na+ channels inactivate
6. Activation of L-type voltage gated Ca2+ channels at -45mV
7. Ca2+ influx - creates plateau phase until Ca2+ channels inactivate - 25Repolarisation of the ventriclesActivation of voltage-gated K+ channels - outward movement of K+
- 26Refractory PeriodAP lasts as long as contraction and this prevents another AP from being initiated therefore the heart cannot exhibit tetany
- 27Cardiac Cycle1. Atrial systole
2. Ventricular systole (isovolumetric contraction, rapid-ejection phase, reduced-ejection phase)
3. Diastole (isovolumetric relaxation, rapid-refilling stage, reduced-refilling stage - 28Atrial systoleOnly accounts for 15-20% of ventricular filling during rest, most done by venous pressure alone, when HR increases, diastole shorterns and atrial contribution is greater
- 29End-Diastolic Volume120-150ml
- 30the effect of EDV on contractionIncreased stretch due to increased EDV increases the strength of the contraction - according to Starling's law and also because more myosin-actin cross bridges are formed
- 31End-diastolic Pressure<10mmHg - it is higher in the left ventricle due to the stiff ventricles because there is a thicker myocardium
- 32Ventricular systole - overview (3)1. Ventricular pressure rises sharply during contraction
2. AV valves close as soon as ventricle pressure exceeds the atrial pressure
3. Represented by QRS complex on ECG - 33P WaveAtrial systole
- 34QRS complexVentricular systole - isovolumetric contraction and rapid-ejection phase
- 35Isovolumetric contractionFor a while both the AV and SL valves are closed while contraction and force builds in the ventricles. This is because ventricle pressure exceeds atria, but doe not exceed aorta and pulmonary artery pressure.
There is no ejection in this stage and the ventricular volume is the same - 36a waveAtrial systole causes an increase in atrial pressure
- 37c wavedue to increased ventricular pressure, the AV valves bulge into the atria, slightly increasing the atrial pressure - this is followed by x descent
- 38Rapid ejection phaseVentricular pressure finally exceeds that of the aorta and pulmonary artery and the SL open
Blood is raidly ejected out of the ventricle into the arteries - 39T wave on ECGReduced ejection phase - ventricles stop actively contacting
- 40Reduced ejection phaseAS contraction wanes, the ejection is reduced. During the 2nd half of ejection the ventricles stop contracting and the ventricular pressure decreases to become less than the aorta and pulmonary artery - flow continues because of momentum.
- 41S1AV valves close as soon as the ventricular pressure exceeds that of the atria
- 42S2During the reduced ejection phase, the flow briefly reverses and this causes the SL valves to close
- 43Dicrotic notchThis is the increase of aortic pressure due to the closure of the SL valves
- 44Diastole - overviewAfter the SL valves close, there is immediate ventricle relaxation
- 45Isovolumetruc relaxationThe AV valves are closed because the ventricular volume is greater than that in the atria
- 46v waveDuring isovolumetric relaxation the atrial pressure increases due to filling
- 47Rapid - refilling phaseVentricle Pressure falls significantly to below atrial and the AV valves open. Ventricular filling is assisted by the elastic recoil of the myocardium
- 48y descentin the rapid refilling stage the AV valves open which causes atrial pressure to fall
- 49Reduced reflilling stageFilling in the 2/3 of diastole is slower and due to venous return alone
- 50End systolic Volume50ml
- 51Ejection fractionSV/EDV = 0.6
HF: <0.5 - 52Ventricular pressure loopStart at 4o'clock and move anticlockwise
1. A
2. Isovolumetric contraction
3. B
4. ejection
5. C
6. Isovolumetric relaxation
7. D
8. Filling - A - 53Ventricular pressure loop measurementsArea: work perfomed
Shape: affected by the ventricular force - affected by EDV and afterload - 54Sharp shape of pulseSmall, stiff (atherosclerosed) artery
- 55S3Heard in young fit people - rapid atrial filling
- 56S3 and S4Occurs when atrial pressure is raised (CHF)
=Gallopp rhythm - 57S4Atrial systole
- 58How is CO altered by a change in CVPIncreased CVP which is only perceived by the RV causes RV SV to increases, this increases pulomnary vascular pressure (which dterines the LV EDP - therefore the LV EDP increases - which increases LV SV (CO)
- 59Affect of sympathetic nervous system on the heart1. Increases HR
2. Increases Cardiac muscle force (without altering stretch - EDV) - increases contractility
3. Increases TPR
4. Increases venoconstriction (decreases compliance, increases CVP, increases blood vol)
Net: Increase in CO - 60Excitation - Contraction CouplingContraction is dependent on intracellular calcium levels
- 61Increased intracellular calcium comes from (2)1. During AP plateau phase - Ca2+ enters the cell and activates Ca2+ sensitive Ca2+ release channels in the SR
2. This allows stored calcium to be released and flood the cytosol (Ca2+ induced - Ca2+ release) - amount of Ca2+ that floods the cytosol is dependent on the amount of Ca2+ stored - 62Relaxation - calciumCa2+ is sequestered into the SR by Ca2+ ATPase
Ca2+ that entered the cell is removed by 3Na+/1Ca2+ exchanger (dependent on the Na+ gradient provided by Na+ ATPase - 63Affect of the SNS on the contractility of the heartNoradrenaline is a positive ionotrope and binds to beta1 receptors on membrane and causes increased Ca2+ entry bia Ca2+ L-type channels - there is more Ca2+ in cytosol.
Also increases Ca2+ sequestration
However, due to the acceleration of HR, there is less time in diastole and less time for sequestation - more Ca2+ is therefore left in the cytosol - Staircase effect - 64InotropesAffect cardiac contractility
1. Postive ionotrope: Noradrenaline, Cardiac glycosides (inhibit the Na+ ATPase that creates gradient for Ca2+ removal)
2. Negative ionotrope: acidosis - H+ competes for Ca2+ binding sites - 65What 3 things is SV dependent on1. Preload
2. Cardiac contractility
3. Afterload - 66Effect of Calcium on troponinAs more Ca2+ enters the cell, it increases the sensitivty of troponin to Ca2+ - therefore there is more force generated from the same amount of intracellular Ca2+
- 67How do vasoconstrictors work1. Binding activates phopholipase C
2. This activate IP3 or DAG
3. Net results in increased calcium entry causing vasoconstriction - 68IP3opens Ca2+ channels on SR allowing entry of Ca2+ from stores
Also stimulates capacitance entry - 69DAG1. Activates Rhokinase and Protein C which mediate calcium sensitisation (more force for same Ca2+)
2. opens receptor operated channels into the cell (Na+/Ca2+ entry into cell) - this causes depolarisation and activate L-type Ca2+ channels - 70VasodilationDecreased intracellular Ca2+:
1. Ca2+ removal by sequestration by smooth endoplasmic reticulum Ca2+ ATPase (SERCA)
2. Ca2+ removal by plasma membrane Ca2+ ATPase (PMCA)
3. Plasma membrane Na+/Ca2+ echange - 71Role of endogenous vasodilatorsNO - stimulates cGMP, stimulates protein kinase G
PGI2, B2 - stimulates cAMP, stimulates protein kinase A
Together these things:
1. Hyperpolarisation of the memrbane - inhibits voltage-gated Ca2+ entry
2. SERCA
3. PMCA - 72NO - Vasodilator (5)1. NO (EDRF - endothelium derived relaxing factor) - synthesised by eNOS in response to increased intracellular Ca2+.
Also synthesised in reponse to bradykinin, histamine, serotonin and neurotransmitter P - 73Other vasodilatorsPGI2
- 74Synthesis of vasoconstricters by the endotheliumET-1
Thromboxane A2 (TXA2) - 75Release of ET-1ET-1 is released in response to
1. Angiotensin
2. ADH
3. Noradrenaline
4. Hypoxia - 76PGI2Shear stress - activates PGI2 to increase flow
- 77Echange vesselscapillaries and small venules
- 78Regulation of Blood flowSmall arterioles are innervated by SNS
Terminal arterioles are innervated by local mediators - that allow perfusion to match metabolism - 79Flow through capillariesThe net hydrostatic pressure is greater than the opposing net oncotic pressure for the length of the capillary there fore there is a net filtration of substances into the interstitium
- 80Protein movement1. Arteriole constriction - decreases capillary perssure, and reabsorbs fluid
2. decreased plasma proteins and loss of endothelial integrity - there is a net infiltration of proteins out of the vasculatures (caused by ischaemia and inflammation) - Also high venous pressures can cause thias - 81Oedema (5)Increased fluid in the interstitial space due to
1)lymphatics are unable to remove fluid quick enough
2)Dysfunctional lymph drainage
3) inflammation - increases permeability and proteins leaks in disrupting the oncotic gradient
4)Not moving - inactivity reduces the muscle pump and increases local venous pressure
5)protein starvation - ascites and enlarged livers - 82Lymphatic drainageLymphatic capillaries - collecting lymphatics - large lymphatics - afferent - lymph nodes - efferent - thoracic duct - subclavian veins
- 83Local control of blood flowArteriolar constriction - in response to stretching and activation of stretch-activated Ca2+ channels in the smooth muscle
(decreased stretch, closes channels = relaxation)
Local vasodilators - increase blood flow, dilutes factors causing vasoconstriction (decreased blood flow allows accumulation) - vasodilation - 84Metabolic factors - effecting hyperaemia1. K+
2. CO2
3. Adenosine
4. Hypoxia - 85K+ - hyperaemiareleased from active tissues in ischaemia - causes relaxation by stimulating the Na+ pump - this increases Ca2+ removal by steepening the gradient that drives the Na+/Ca2+ exchanger
= hypolarisation - 86CO2 - hyperaemiaHypercapnia causes vasodilation by stimulating increased NO production and inhibiting smooth muscle Ca2+ entry
- 87AdenosineVasodilator released from the heart, brain and skeletal muscle during metabolism and hypoxia, it increases cAMP in smooth muscle
Produced from AMP - 88Hypoxia - hyperaemiareduced ATP therefore K+ ATPase channel activation causing hyperpolarisation
katp? - 89Autocoids - hyperaemia/hypoaemiaInflammation - histamine and bradykinin - vasodilation and increased permeability of exchange vessels - allowing the entry of leucocytes and antibodies
Platelet activation - releases vasoconstrictors - serotonin and TXA2 - decrease blood loss - 90Special circulations (5)1. Skeletal muscle
2. Brain
3. Skin
4. Pulmonary circulation
5. Coronary circulation - 91Skeletal muscle - circualtionSkeletal muscle provides major contribution to TPR. At rest most capillaries are not perfused, arterioles are constricted.
During exercuse and metabolic hyperaemia caused by release of K+ and CO2 and adenosine - overrides sympathetic vasoconstriction in the working muscle. Adenosine also reduces blood flow to non-working muscles to conserve CO - 92Brain - special circulationCO2 and K+ are important metabolic regulators in the brain - increases cause functional hyperaemia which links blood flow to activity
Hyperventillation reduces PCO2 and can cause fainting due to cerebral vasoconstriction - 93Coronary circulation - special circulationincreased oxygen demand is met by increased flow caused by adenosine, K+ and hypoxia - it overrides vasoconstriction mediated by sympathetic nerves and is assissted by circulating adrenaline which causes vasodilation via beta2-adrenergic receptors
- 94Skin - special circulationsTemperature effects vasodilation/vasoconstriction - sweating activated by sympathetic cholinergic fibres releases bradykinin - which is a vasodilator
- 95Pulmonary circulation - special circulationmost important factor regulating flow is hypoxia (hypoxic pulmonary vasoconstriction) - causes small arteries to constrict (hypoxia usually causes vasodilation) - it diverts the blood away from poorly ventillated areas of the lung to maintain the optimal ventillation/perfusion matching.
Deterimental effects in lung disease: pulmonary HTN
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- Karteikarten am Module 2.06 physiology , erstellt von rachelburton23 am 13/06/2015.
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