Physiology 8 - Dr James Brown PDF

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Dr James Brown...

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Physiology 8 – Cardiac Physiology The heart is a dual-pump Two halves, four chambers Both sides simultaneously pump equal amounts of blood Two systems; Pulmonary functions – to the lungs Systemic circulation – to the rest of the body Heart Valves Pressure-operated heart valves ensure that blood flows in the right direction through the heart Preload – pressure exerted on the wall of the ventricles before they eject blood Afterload – pressure of blood in the blood vessels, which ventricles are pumping against Because blood pressure is already high, you can imagine there is more blood returning the heart It must work constantly hard to maintain cardiac homeostasis The resistance the heart has to overcome because blood pressure is so high Atrioventricular valves: valves between the atria and ventricles Let’s blood flow from the atria into the ventricles during ventricular filling Prevents backflow from the ventricle to the atria during ventricular emptying Left valves  Bicupsid valves Right valves  Tricupsid valves Semilunar Valves: Aortic Valves Pulmonary Valves These are the arteries leaving the heart

Electrical Activity Electrical signals drive the muscle contraction that ejects the blood out of the heart The heart contracts rhythmically as a result of action potentials that it generates itself The heart is made up of two types of cells: - Contractile cells: 99% of the cardiac muscle, do the mechanical work of pumping - Autorhythmic cells: initiate and conduct the action potentials Resting potential membrane = Autorhythmic Cells high K+ inside the neurone, and - Within the SA node a lot of Na+ outside. When these - Pacemaker potential in autorhythmic cells ions diffuse across these o Complex interactions of several ionic mech membranes that you get a - Action potential in autorhythmic cells higher overall charge and you o Rising phase of the action potential occurs in response to activation of voltage gated Ca2+ channels o Allows the heart to always be ready for the next contraction

The spread of cardiac excitation is coordinated so that the pumping stays efficient And that it can pump blood out without any resistance and inconsistences - Atrial excitation and contraction must be complete before ventricular contraction starts – delay of 0.09 sec - Excitation of cardiac muscle fibres must be coordinated so that each component of the heart chamber contracts as a unit - The pair of atria and pair of ventricles should be coordinated so that they contract simultaneously - Contract from the bottom up – purkinje fibres

Atrial Excitation - Interatrial pathway - Internodal pathway Conduction between the atria and the ventricles - Atrioventricular nodal delay Ventricular Excitation - Is crucial for hastening speed of excitation in ventricles Electrical Structures - SA node o Normal pacemaker of the heart - Atrioventricular node - Bundle of His (i.e. atrioventricular bundle) - Purkinje fibres Action Potential - Driven by movement of ions across a membrane o This is driven by permeability - Action potential of contractile cardiomyocytes (heart cells) shows a ‘plateau’ o Plateau phase – membrane potential is close to its peak positive level (maximum) for several hundred milliseconds - Calcium entry from the ECF o Induces a much larger Ca2+ release from the sarcoplasmic reticulum Overview - A long refractory period prevents tetanus (spasms) of cardiac muscle o Allows time for the ventricles to empty and refill prior to the next contraction - ECG is a record of the overall spread of electrical activity through the heart o Electrical activity present in body fluids from the cardiac impulse that reaches the body surface and is detected The heart; contracts to empty (systole) relaxes to fill (diastole) P wave = atrial depolarisation – bit of the atria being actively stimulated PR segment = AV nodal delay – the electrical impulse being sent to the AV node is delayed, so that the atria can contract together QRS segment = ventricular depolarisation – not ventricular contraction, when they are being stimulated but not t t d t

Diastole - 80 Filling of the heart 1. pressure in the ventricles decrease from the systolic 2. the pressure in the left ventricle is less than the pressure in the left atrium the (atrioventricular/bicuspid) mitral valve opens allowing blood flow 3. early diastole is a suction mechanism – 80% of blood flow 4. late diastole is due to atrial contraction (atrial kick) 20% of blood flows passively down the ventricles during this kick 5. the amount of blood in the ventricles before ejection is called; End Diastolic Volume (EDV) Systole - 120 Contraction/ejection of the heart 1. as ventricles contracts, ventricular pressure increases rapidly the pressure exceeds the atrial pressure 2. forces AV valve to close (preventing backflow)

a. but not high enough to open the semi-lunar valve 3. aortic pressure exceeds ventricular pressure aortic valve remains closed ventricle cannot empty despite its contraction 4. for a brief moment, all valves are closed (isovolumetric ventricular contraction) 5. rapidly increasing ventricular pressure exceeds aortic pressure 6. forces aortic valve to open and ventricular ejection begins 7. ejection is fast at first then slows down 8. amount of blood in the ventricle after ejection is called; End Systolic Volume (ESV) Cardiac Output - the volume of blood being pumped by the heart - Cardiac Output = Stroke volume * Heart Ra CO = SV * - Heart rate is determined by automatic influences on the SA node o Parasympathetic (rest and digest) and sympathetic stimulation (fight or flight - increase contractility) on the heart

Stroke Volume - Determined by the extent of venous return and by sympathetic activity o Intrinsic control  venous system  If the amount of blood entering the ventricle is the same as the amount leaving the heart  Amount of blood coming in also affects the force at which the ventricles will contract – Frank Sterling Law o Extrinsic control:  sympathetic stimulation of the heart - Terminology:

o Preload – the degree to which the ventricles are stretched prior to contracting (EDV) o Afterload – the pressure that the chambers of the heart must generate in order to eject blood out of the heart

Controlling Stroke Volume - Increased end-diastolic volume results in increased stroke volume - Intrinsic control of stroke volume: heart’s inherent ability to vary SV - Frank-Starling Law: intrinsic relationship between EDV and EV - Advantages and mechanism of the cardiac length-tension relationship

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Sympathetic stimulation increases the contractibility of the heart o Contractibility  strength of contraction at any given EDV Stroke volume can be graded by varying; o the initial length of the muscle fibres o the extent of sympathetic stimulation...