Lecture 7-Mechanical Activity of the Heart & Heart Failure (2023) PDF

Mechanical Activity of the Heart and Introduction of Heart Failure in Comparison to Physiological State Dr. dr. Denny Agustiningsih, M.Kes., AIFM., AIFO-K dr. Dyah Adhi Kusumastuti, Sp.JP Learning Objectives 1. Explain the relationship between electrical activity and mec...

Mechanical Activity of the Heart and Introduction of Heart Failure in Comparison to Physiological State Dr. dr. Denny Agustiningsih, M.Kes., AIFM., AIFO-K dr. Dyah Adhi Kusumastuti, Sp.JP Learning Objectives 1. Explain the relationship between electrical activity and mechanical activity of the heart. 2. Explain the mechanism of contraction and relaxation of the heart muscle 3. Describe the cardiac cycle and the influenced factors 4. Describe the distribution of cardiac output and the influenced factors 5. Electric activity of the heart: Electric impulse generation and spreading in the heart and its role in cardiac muscle contraction and how the cardiac muscle contracts. 6. Mechanical activity of the heart: cardiac cycle (systolic and diastolic phase), the Frank-Starling mechanism, heart sounds, refractory period and cardiac output 7. Electrocardiograph: use ECG properly and take electrocardiograph recording. 8. Introduction of heart failure in comparison to physiological state MECHANICAL ACTIVITY OF THE HEART “heart as a pump” DENNY AGUSTININGSIH [email protected] Mechanism of Cardiac Muscle Excitation, Contraction & Relaxation During the plateau phase of cardiac worker cells electric activity Ca ion influx through L-type Ca channels Triger Ca released from the sarcoplasmic reticulum Role of the RYR, Calcequestrin, triadin dan junctin Ca ions bind with troponin C in the myofibrils Mechanism of Cardiac Muscle Relaxation At the end of the plateau of the cardiac action potential, the influx of Ca ions to the interior of the muscle fiber is suddenly cut off, the Ca ions in the sarcoplasm are rapidly pumped back out of the muscle fibers into both the sarcoplasmic reticulum and the T tubule– extracellular fluid space. Transport of Ca back into the sarcoplasmic reticulum is achieved with the help of a Ca- ATPase pump (SERCA) Role of phospholamban Ca ions are also removed from the cell by a Na- Ca exchanger. The Na ions that enter the cell during this exchange is then transported out of the cell by the Na-K ATPase pump. As a result, the contraction ceases until a new action potential comes along. STRENGTH OF CONTRACTION Sarcomeres are not “all or none” as in skeletal muscle The response is graded Depends on Ca2+ level in the cytosol Strongest contraction when stretched 80-100% of maximum (physiological range)  THE CARDIAC CYCLE What is the cardiac cycle? the sequence of events that occur when the heart beats. Changes in volume and pressure of the chambers Open and close valves Heart sounds Repetitive contraction (systole) and relaxation (diastole) of heart chambers Blood moves through the circulatory system from areas of higher to lower pressure 🡪 from LV to RA CARDIAC CYCLE : WIGGER’s DIAGRAM Relationship between electric (ECG), pressure & volume changes, heart sound, cardiac cycle Preload Represents the “load” placed on the muscle fibers before they contract Frank-Starling law states “Stroke volume increase as EDV (ending diastolic volume) increases – stretch 🡪 more force” EDV is determine by venous return Venous return is affected by Skeletal muscle pump Respiratory pump  CARDIAC OUTPUT The amount of blood the heart pumps in 1 minute Controlled to maintain the proper amount of flow to tissues Stroke Volume and Heart Rate Determine Cardiac Output Factors Affecting Stroke Volume Contractility the intrinsic ability of cardiac muscle to develop force for a given muscle length. Affected by inotropic agent Preload the muscle length prior to contractility dependent upon ventricular filling (or end diastolic volume/EDV) Afterload the tension (or the arterial pressure) against which the ventricle must contract. Depends on the diameter and elasticity of the vessel’s wall Cardiac Output Distribution & Cardiac Reserve Cardiac reserve: extra volume that the heart can pump beyond the normal resting condition 3-4 x Cardiac output Increase: athletes Decrease: age, pathologic condition WHAT HAPPENED IN HEART FAILURE? Pressure-Volume Loop Pathophysiology The etiologies can be grouped into those that (1) impair ventricular contractility, (2) increase afterload (3) impair ventricular relaxation and filling. Heart failure that results from an abnormality of ventricular emptying (due to impaired contractility or greatly excessive afterload) is termed systolic dysfunction Heart Failure caused by abnormalities of diastolic relaxation or ventricular filling is termed diastolic dysfunction Lilly LS. Pathophysiology of Heart Disease. 2016  1. Systolic Dysfunction End-systolic pressure-volume relation (ESPVR) shifted Pressure downward and rightward Increase end-systolic volume Increase end-diastolic volume  2. Diastolic dysfunction Diastolic pressure-volume curve shifted upward Pressure Increased end-diastolic pressure Decreased end-diastolic volume Compensantory Mechanism 1. Frank-Starling Mechanism 2. Neurohormonal response 3. Ventricular Hypertrophy and Remodelling The radius of the ventricular chamber therefore enlarges, doing so in proportion to the increase in wall thickness, and is termed eccentric hypertrophy. Chronic pressure overload (e.g., caused by hypertension or aortic stenosis) results in the synthesis of new sarcomeres in parallel with the old (i.e., the myocytes thicken), termed concentric hypertrophy. Januzzi JL., Braunwald’s Heart Disease. 2019 Reference David Miranda, Gregory D. Lewis, Michael A. Fifer. Heart Failure. In : L. S. Lilly (ed). Pathophysiology of Heart Disease. 6th edition. Wolters Kluwer.