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Intrinsic And Extrinsic Control Of The Heart Notes

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Intrinsic and extrinsic control of the heart
-pumping of blood through the heart is measured by cardiac output- volume of blood ejected by one ventricle in one minute
-cardiac output is determined by stroke volume (70ml) and heart rate (70bpm) so resting cardiac output is 5l/min
-the cardiac output can be modulated by intrinsic and extrinsic factors- during excercise 20 or 30 L/min Measuring cardiac output a)Fick principle- based on mass observation
-the whole body consumption of O2 in a resting individual is measured using a spirometry
- O2 content is also measured by measuring oxygen content in mixed venous blood from the right ventricle or pulmonary trunk (cardiac catheterisation) and arterial blood (from radial artery)- this tells us the amount of oxygen consumed per litre of blood
-cardiac output = oxygen consumption per minute/(arterial-venous oxygen concentration) 250mls O2 consumed per minute/ 50mls of Oxygen extracted per litre of blood 5L/minute b) Doppler measurement
-measures ultrasound pulses- estimates aortic flow non invasively c)Echocardiography- ultrasound technique. End diastolic and systolic volumes - This is used to calculate stroke volume and measurements of HR through counting of pulses leads to cardiac output Electrical excitation of the heart
-heart rate is set myogenically by regular firing of action potentials by SAN. The rate of firing can be modulated by sympathetic/ parasympathetic input
-electrical excitation passes to the atria, then the AV node, then the bundle of his and purkinje fibres, then ventricular myocytes
-the spatial behaviour of the propagating can be recorded on the ECG Excitation- contraction coupling mechanisms of contraction

-cardiac muscle is an electrical synctium- intercalated discs- connexion based Gap junctions and desmosomes, action potentials propagate through these gap junctions
-action potentials travel down the T tubules which have travel radially, but unlike skeletal muscle travel axially as well- the propagating action potentials causes the opening of voltage gated calcium channels in the T tubules- influx of calcium-trigger calcium in the dyadic spaces
-Excitation-contraction coupling- requires Ca influx through L type Ca channels unlike skeletal muscle where there is mechanical coupling. The L type calcium channels have an open probability of 0.1 so there are 20-100 L type channels on the sarcolemma. The Sarcoplasmic reticulum is positioned directly under these calcium channels- trigger calcium binds to Ryanodine 2 receptors (ryanodine 1 receptors are found in skeletal muscle) which open calcium channels and permits calcium stored in Sarcoplasmic reticulum to flux into the cytoplasm-calcium induced calcium release
-the ryanodine receptors are found all over the sarcoplasmic reticulum so by positive feedback, calcium released by one ryanodine receptor leads to the opening of more calcium channels that are coupled to the ryanodine receptors
-the calcium binds to cardiac isoform of troponin C - TNNC1. The Ca-TNNC1 releases the inhibition of the cardiac isoform of troponin on actin. The tropomyosin filaments bound to cardiac troponin T to shift away. This allows myosin to interact with the active sites on the Actin ATP fuels cross bridge cycling and thick filaments slide past the thin filaments and generates tension. Relaxtion of the cardiac muscle a)extrusion of calcium into the extracellular fluid
-when the membrane potential returns to more negative values, and the calcium concentration falls
-Na/Ca exchanger which pumps 3 sodium in and one calcium out
-Sarcolemmal calcium pump b)reuptake of calcium from the cytosol by SR
-calcium pump in the sarcoplasmic reticulum.
-unlike skeletal muscle the SR calcium pump is inhibited by phospholamban. When phosphorylated by cyclic dependent protein its ability to inhibit SR calcium pump is lost c)dissociation of calcium from Troponin C
-as calcium concentrations fall, calcium dissociates from troponin C and blocks the actin myosin interactions and causes relaxation. Adrenergic agonists increase the rate of relaxation by promoting phoshphorylation of troponin I which enhance the dissociation of calcium from troponin C.

Intrinsic control of the heart

Intrinsic control factors mostly affect cardiac output by varying the stroke volume by affecting the myocardial contractility This can be either heterometric (changes in the sarcomere length) or homometric (independent of the cell length and is controlled by agents such as Na, Ca, pH)

Heterometric intrinsic control a) Frank starling mechanism: intrinsic control of stroke volume- increase in stroke volume following increase in central venous pressure denervated isolated frog heart, with ligated aorta, was pumped with blood using artificial lung apparatus,warm oxygenated blood from a venous reservoir, heigh of the reservoir controlled the central veounous presure- an increase in preload lead to increase in cardiac output
-factors affecting central venous pressure: pressure= blood volume/compliance
-blood volume
-decrease in cardiac output leads to blood backing up into the venous circulation as less blood is pumped into the arterial circulation- this increases blood volume
-increase in blood volume due to renal failure
-increase in blood volume when a person goes from standing to supine position
-compliance :
-venous constriction due to sympathetic activation or circulating vasoconstrictors-contraction of smooth muscle within veins which increases vascular tone and decreases compliance
-compliance also decreases due to forced expiration- as the intrapleural pressure rises there is external compression of the venacava.
-muscle contraction of the lower limbs compresses veins and decreases compliance
-increased preload/diastolic filling pressure to the heart, caused by increased central venous pressure (increased blood volume or venous constriction) - this raises the volume of blood loaded into the right atrium, then right ventricle- this increases the loading pressure into the left atrium and left ventricle
-Increased loading of the blood stretches the myocytes in the walls of the cardiac chambers- this increases the force of contraction - increase in developed pressure (systolic - diastolic) when activated by an action potential

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