Marie Nováková, Department of Physiology1 CARDIAC MECHANICS HEART AS A PUMP CARDIAC CYCLE HEART FAILURE Marie Nováková, Department of Physiology 2 CARDIAC OUTPUT (CO) CO HR SV CO = HR x SV CORONARY FLOW EDV Venous return Compliance Aortal pressure LV = RV SV = EDV - ESV Ejection fraction EF = EDV – ESV / EDV 5l/min 70ml >60% REGULATION ANS AUTOREGULATION of cardiac contraction Heterometric: Starling law Homeometric: Frequency effect CONTRACTILITY Ability to contract Depends on tissue perfusion (substrates and oxygen supply for ATP production; Ca2+ availability) Marie Nováková, Department of Physiology3 Fuyu Kobirumaki-Shimozawa et al., J Physiol Sci (2014) 64:221–232 STARLING LAW Marie Nováková, Department of Physiology4 Fuyu Kobirumaki-Shimozawa et al., J Physiol Sci (2014) 64:221–232 Marie Nováková, Department of Physiology 5 Henry Pickering Bowditch (1840 – 1911) HOMEOMETRIC AUTOREGULATION (FREQUENCY EFFECT) During increasing HR (stimulation frequency) the force of developed contraction rises Ratio between intra- and extracellular calcium concentrations increases Marie Nováková, Department of Physiology 6 0,5 Hz 2 Hz1 Hz 3 Hz Marie Nováková, Department of Physiology7 Marie Nováková, Department of Physiology8 CARDIAC RESERVE = maximal CO / resting CO CORONARY RESERVE = maximal CF / resting CF CHRONOTROPIC RESERVE = maximal HR / resting HR VOLUME RESERVE = maximal SV / resting SV 4 - 7 3,5 3 - 5 1,5 CO = cardiac output CF = coronary flow HR = heart rate SV = stroke volume Marie Nováková, Department of Physiology9 CARDIAC RESERVE CO (l/min) WORKLOAD (W/kg) ATHLETHS HEART PHYSIOLOGICAL RESPONSE HEART FAILURE 1 2 3 4 10 30 20 Marie Nováková, Department of Physiology10 IMPORTANT TERMS Length-tension relationship (curve) Minimal length l0 Passive, active, total force Optimal length Isometric, isotonic, auxotonic contraction Autoregulation of contraction – heterometric (Starling) Preload, afterload Marie Nováková, Department of Physiology11 Passive tension, active tension, isometric contraction, isotonic contraction, auxotonic contraction Marie Nováková, Department of Physiology12 AFTERLOADED CONTRACTION PRELOAD, AFTERLOAD 1 2 3 4 AP PRELOAD (~ enddiastolic filling) AFTERLOAD (~ pressure which must be developed) stimulus Marie Nováková, Department of Physiology13 P (mmHg) V (ml)50 120 10 100 80 125 A B C D ESV (RV) EDV Work of the heart = P . V LAPLACE law: T = P . r / 2h P = T . 2h / r AB – isovolumic contraction BC – ejection CD – isovolumic relaxation DA – filling CARDIAC CYCLE – P-V LOOP Marie Nováková, Department of Physiology14 P = T . 2h . r –1 Isovolumic contraction: T rises up, valves closed – increase in P P = T . 2h . r –1 Ejection: r decreases, h rises, thus P increases (even at the same T) P = T . 2h . r –1 Isovolumic relaxation: T decreases, valves closed – decrease in P P = T . 2h . r –1 Ventricular filling: r and T rise, P first falls down, then rises up (length/tension relationship) Marie Nováková, Department of Physiology15 INCREASED PRELOAD MODEL Marie Nováková, Department of Physiology16 INCREASED AFTERLOAD MODEL Marie Nováková, Department of Physiology17 INCREASED PRELOAD AND AFTERLOAD MODEL Marie Nováková, Department of Physiology18 HEART SOUNDS Caused by vibration of various anatomical structures and event. blood: • Closure and stretching of valves • Isovolumic contraction of heart muscle (papillary muscles, tendons) • Turbulent blood flow Vibration of ventricular wall I. – mitral (+ tricuspidal) valve closure II. - aortal (+ pulmonary) valve closure III. - fast filling of ventricles - pathological IV. - contraction of atria – mostly pathological Z mitral valve aortal valve I. II. III. IV. C C O O O – open, C - closed Splitting of I. or II. sound: asynchronous closure of M - T valve (I.) or Ao - P valve (II.) (inspiration, hypertension….) Marie Nováková, Department of Physiology19 Z mitral valve aortal valve I. II. Z Z O O O – open, C - closed systole diastole PHYSIOLOGICAL SOUNDS AORTAL STENOSIS MITRAL REGURGITATION MITRAL STENOSIS AORTAL REGURGITATION MURMURS – pathological phenomena based on turbulent blood flow 1. SYSTOLIC • Stenosis – aortal, pulmonary (1) • Regurgitation – mitral, tricuspidal (2) 2. DIASTOLIC • Stenosis – mitral, tricuspidal (3) • Regurgitation – aortal, pulmonary (4) 3. SUSTAINED: • Defects of septum Marie Nováková, Department of Physiology20 POLYGRAPHY (polygram) Phases of the cycle Aortic pressure LV pressure LA pressure LV volume valve closed Carotid sphygmogram ECG Phonocardiogram Marie Nováková, Department of Physiology21 HEART FAILURE = loss of cardiac reserve The heart is not able pump sufficient amount of blood into periphery at normal venous return. SYMPTOMS fatigue, oedemas, venostasis, dyspnoea, cyanosis ACUTE x CHRONIC. COMPENSATED x DECOMPENSATED. MOST FREQUENT CAUSES: • Severe arrhythmias • Overload – volume (aortal insufficiency, a-v shunts) or pressure (hypertension and aortal stenosis – left overload, pulmonary hypertension and stenosis of pulmonary valve – right overload) • Cardiomyopathy CO (l/min) WORKLOAD (W/kg) ATHLETHS HEART PHYSIOLOGICAL RESPONSE HEART FAILURE 1 2 3 4 10 30 20 Marie Nováková, Department of Physiology22 ACUTE FAILURE CARDIOGENIC SHOCK COMPENSATION CHRONIC FAILURE SUDDEN DEATH DECOMPENSATION GRADUAL LOSS OF CARDIAC RESERVE COMPENSATION Marie Nováková, Department of Physiology23 BAROREFLEX Physiological role: compensation of decrease in minimal volume of circulating fluids Signal: BP decrease (orthostase, work vasodilatation) Sensor: baroreceptors Response: activation of SAS (increased HR, inotropy, BP) Pathological signal: long-lasting decrease of BP due to heart insufficiency Results: increased energy outcome – vicious circle ACTIVATION OF RAAS Physiological role: compensation of loss of circulating fluids (bleeding) Signal: decrease in renal perfusion Sensor: juxtaglomerular system of kidney Response: BP increase (angiotenzin II.), water retention (aldosteron) Pathological signal: decrease in renal perfusion due to heart insufficiency Results: increased preload and afterload, increased energy outcome – vicious circle HEART FAILURE - COMPENSATION Ca2+ - antagonists b – sympatolytics angiotenzin-converting enzyme inhibitors (AT II. receptors) Marie Nováková, Department of Physiology24 DILATATION (STARLING PRINCIPLE) Physiological role: compensation of momentary right-left differences Signal: orthostase, deep breathing, beginning of exercise Pathological signal: continual blood stasis in the heart Results: increased energy outcome – vicious circle HYPERTROPHY Physiological role: preservation of energetically demanding tension of ventricular wall Signal: P = s . 2 h / r, intermittent BP increase (athletes heart) Response: concentric remodelling Pathological signal: continual increase of preload or afterload Results: worsening of oxygenation, fibrotisation – vicious circle cardiac glycosides (digitalis)diuretics