Cardiac muscle physiology

Learning objectivesBy reading this article, you should be able to:•Recall the principal ion channels and currents involved in cardiac action potential.•Describe mechanisms underlying excitation-contraction coupling.•Relate structure of myofilaments to their function health disease.•Discuss metabolic pathways that provide energy for muscle contraction.Key points•Resting membrane potential arises from ionic concentration gradients across cell coupled with varying permeability each ion. Potassium has dominant influence because its high permeability.•The characteristic shape is a result distinct sodium, calcium potassium channels. Genetic variants affecting these have been linked numerous congenital arrhythmia syndromes.•Type 2 ryanodine receptor plays central role calcium-induced release activation coupling.•Abnormalities cellular handling myofilament identified as important cardiomyopathies heart failure.•An understanding remodelling energetics failure may future therapeutic options. By contraction. •Resting The biomechanical pump at centre our circulatory system. It contracts rhythmically approximately 6 weeks gestational age until death.1Valenti O. Di Prima F.A.F. Renda E. et al.Fetal during first trimester pregnancy.J Prenat Med. 2011; 5: 59-62Google Scholar Contractions are initiated by potentials, arising pacemaker cells, transmitted individual cardiomyocytes via specialised conduction pathways, through intercalated discs gap junctions between cells.2Nerbonne J.M. Kass R.S. Molecular physiology repolarization.Physiol Rev. 2005; 85: 1205-1253Google arrival electrical signal results coupling, sarcomere shortening ejection blood.3Bers D.M. Cardiac coupling.Nature. 2002; 415: 198-205Google In article we describe processes mechanics contraction metabolism fuelling activity. 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Em: potential; P: membrane; P’: total all (PT); “x”. At rest, P’Na, P’Ca P’Cl very low while P’K relatively high, therefore Em closest K+.4Klabunde Under conditions K+ moving out Na+ diffusing in, down (Table 1). maintained series ion-exchange mechanisms. Na/K-ATPase transports 3 contributing negative well differential concentrations.4Klabunde There also Na–Ca exchanger (NCX) which exchanges generating small current operate either direction, depending on phase (favouring efflux diastole influx when more positive than – 20 mV).Table 1Intracellular concentrations ScholarIonIntracellular (mmol L-1)Extracellular L-1)K+1504Na+20145Ca2+0.00012.5Cl-4120 Open table new tab originates function, ability generate regular, spontaneous potentials. Cells sinoatrial (SA) node (70–80 beats min−1), atrioventricular (AV) (40–60 bundle His Purkinje fibres (15–40 min−1) capable activity.7Guyton A.C. Hall J.E. Rhythmical excitation heart.in: Guyton Textbook Medical Physiology. 11th ed. 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As mentioned, regional duration example endocardium epicardium (Fig 1), especially Ito.5Varró ensures one-way preventing re-entrant circuits. disease, changes propagation refractory period give rise formation substrate, combined trigger dangerous re-entry tachycardia.5Varró Such triggers ectopic early after-depolarisations, commonly reactivation SR leading depolarising respectively.5Varró When reaches cardiomyocyte, [Ca2+] triggered, proteins, actin myosin 3), sarcomeric thus shortening. force contraction, inotropy, mass depends sensitivity Ca2+.3Bers Thus control inotropy regulate affect actin-myosin interaction.3Bers Numerous T-tubule invaginations sarcolemma ensure complete synchronous core loss contributes dysfunction.15Eisner D.A. Caldwell J.L. Kistamás K. Trafford A.W. 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