Title physiology 2.pdf ✅

OSAMA AKL MRCOG COURSE physiology Physiology
OSAMA AKL MRCOG COURSE physiology The heart Pregnancy-specific changes in the cardiovascular system ● Plasma volume is increased by 45–50 % ● Blood volume is increased by 40 % ● Heart rate increases by 10–20 bpm (by 32 weeks) ● Cardiac output is increased by 30–50 % (by 24 weeks) ● Systemic vascular resistance (SVR) is reduced by 20–30 % ● Dilutional decrease in colloid oncotic pressure ● Central venous pressure is unchanged • RBCS increase 18 % Distribution of COP during pregnancy Uterus 400 ml/min Kidney 300 ml/min Skin 500 ml / min Git - breast 300 ml/min Characteristics of the cardiac muscle cell Skeletal muscle Cardiac muscle Can have tetany yes no Action potential short long Plateau phase short long ● Regular contracting ventricular fibers have a stable resting membrane potential (phase 4), unlike the specialized pacemaker and conducting fibers, which have unstable resting membrane potentials. ● one electrical event per mechanical event. Membrane channels The cardiac muscle cell membrane has channels for K +, Na +, and Ca 2 + ions. Un-gated K + channels ● always open - always an efflux of K. K + equilibrium potential is never reached. Na Ca K
OSAMA AKL MRCOG COURSE physiology Voltage-dependent (gated) K + channels ● open at rest. ● They are closed during the plateau phase ● They re-open with repolarization. Voltage-dependent (gated) Na + channels ● closed at rest. ● open quickly and close quickly. ● open during depolarization. Voltage-dependent (gated) Ca 2 + channels ● closed at rest. ● With depolarization they open and remain open during the plateau phase. Cardiac muscle action potential Phase 0 (depolarization) ● Fast Na + channels open, Na + influx into the cell. Phase 1 (slight repolarization) ● This is thought to be due to special K + rather than Cl – channels. Phase 2 (plateau) ● The slow voltage-dependent Ca 2 + channels are open, resulting in Ca 2 + influx into the cell (contractile response) and also triggers additional Ca 2 + release from intracellular storage in the sarcoplasmic reticulum. ● Voltage-dependent K + channels are closed (only the un-gated channels are open, so K + conductance is low allowing just the usual efflux of K + but no more). The Ca 2+ influx balances the K + efflux, which produces the stable plateau phase and delays repolarization. ● The closure of the voltage-dependent K + channels ensures that there is no massive efflux of K +, adding to the delay in repolarization Phase 3 (repolarization) ● The voltage-dependent Ca 2 + channels close, stopping Ca 2 + influx. ● Voltage-dependent K + channels re-open, thereby increasing K + efflux and causing repolarization. Action potential characteristics of (SA and AV nodes and Purkinje fibers) 1. Unstable phase 4 (pacemaker pre-potential) with gradual depolarization towards threshold. This leads to the cell depolarizing automatically. 2. Depolarization is not due to Na + influx through fast channels but probably to Ca 2 + influx through slow channels. 3. Repolarization is due to the efflux of K + like any other action potential. 4. The SA nodal fibers are innervated by sympathetic and parasympathetic neurons.
OSAMA AKL MRCOG COURSE physiology ● Sympathetic: increasing the intrinsic firing rate. ● Parasympathetic: slowing down the intrinsic firing rate. ● SA nodal cells have the fastest intrinsic rate, with AV nodal cells being next fastest, and the Purkinje fibers have the slowest intrinsic rate. ● the Purkinje cells are the fastest conducting fibers, whilst the AV node cells are the slowest. ● Preload : ventricular muscle end of diastole stretch. Technically, it is equal to left ventricular end diastolic volume or pressure, but clinically it is more easily measured by the pulmonary capillary edge pressure. ● Left ventricular afterload is the force that the muscle must generate to eject the blood, measured by the mean aortic pressure. Afterload is increased in hypertension and decreased in hypotension. ● The Frank–Starling relationship: is the effect of preload on sarcomere length. (increased venous return increases EDV ,increasing the contraction). ● increased contractility implies more and quicker supply of Ca 2 + to the contractile machinery. Control of heart rate ● The intrinsic heart rate: 110 bpm. ● Under resting conditions there is usually a parasympathetic tone to the SA and AV nodes through the right and left vagus nerves, which reduce the basal rate. ● Sympathetic stimulation leads to tachycardia and increased contractility. Baroreceptor reflex and blood Pressure regulation ● The carotid sinus stretch receptors are much more important than their aortic arch counterparts. ● The glossopharyngeal cranial nerve IX is continuously firing information on blood pressure into the CNS. ● If blood pressure (BP) increases (hypertension) or decreases (hypotension) then the afferent CNS input increases or decreases respectively. ✓ The parasympathetic : runs only to the heart to alter the heart rate and thereby change the cardiac output. ✓ The sympathetic arm exerts a more complex series of effects on the: 1. heart — increasing the cardiac output - heart rate - contractility 2. arterioles — increasing the TPR but only in non-essential tissues, e.g. skin, resting skeletal muscle, and kidneys (there is no effect on the brain or coronary circuits) 3. Veins — venoconstriction and changing the amount of blood stored in the reservoir. ECG changes with pregnancy: 1. LVH & dilatation 2. Apex is shifted upwards left