The Cardiac Cycle 2023 PDF

The cardiac revolution To function like a pump, the heart repeats 2 successive phases: ⮲ Depolarization of cells causes systole = contraction. ⮲ Repolarization of cells causes diastole = relaxation to fill the atria and ventricles. A cardiac cycle therefore comprises an alternation of...

The cardiac revolution To function like a pump, the heart repeats 2 successive phases: ⮲ Depolarization of cells causes systole = contraction. ⮲ Repolarization of cells causes diastole = relaxation to fill the atria and ventricles. A cardiac cycle therefore comprises an alternation of electrical and mechanical phenomena. The two mechanical phenomena are : - systole: contraction of the 2 ventricles and ejection of blood - diastole: relaxation and filling of the 2 ventricles cycle The cardiac revolution is the period between the end of one cardiac contraction and the end of the next. Normally, the duration of ventricular diastole (DV) is greater than the duration of ventricular systole (SV). This SV/DV variation is a function of heart rate (Figures 1 and 2). Figure 1. The cardiac Revolution Within normal heart rate limits (Fc), flow increases with frequency (Figure 2 and Table 1). Above a maximum age-dependent frequency (220 - age), flow peaks, followed by a rapid decrease in end-diastolic volume. The consequences of this phenomenon are : - greater adaptation of cardiac output to exercise in trained athletes, since their resting heart rate is lower PAGE 1  - prolonged tachycardia (high heart rate) progresses to heart failure Figure 2. Duration of cardiac mechanical phenomena as a function of heart rate Tableau 1. Cardiac cycle duration VENTRICULAR SYSTOLE (FIGURE 3) − It begins with the closure of the atrioventricular (A-V) valves. It comprises 2 parts: − - Iso-volumetric ventricular contraction (at constant ventricular volume): sigmoid valves still closed - Systolic ejection: opening of the sigmoid valves, blood is expelled into the aorta and pulmonary artery. Arterial and ventricular pressures rise in parallel. Ventricular volume: decreases. This phase ends when the sigmoid valves close. Figure 3. Ventricular systole PAGE 2 VENTRICULAR AND GENERAL DIASTOLE (FIGURE 4) - It begins with the closure of the sigmoid valves and comprises 4 stages: - - Iso-volumetric relaxation: closure of the sigmoid valves while the A-V valves are still closed and the cardiac muscle relaxes. - - Ventricular filling: this takes place in three stages: 1. Rapid passive filling Following ventricular relaxation, a post-systolic vacuum is created, causing the A-V valves to open and suctioning the atrial contents. 2. Slow passive filling (diastasis): ventricular pressures and volumes change little, and intra-atrial volume decreases. This stage plays a significant role in long cardiac cycles. 3. Active filling (atrial systole): completes ventricular filling. It plays a hemodynamic role during acceleration of Fc and if blood flow is obstructed. Figure 4 : Ventricular and general diastole Hemodynamic phenomena during a cardiac cycle VENTRICULAR FILLING In the left ventricle (LV), this takes place between the opening and closing of the mitral valve, and reduces the ventricular volume from 45 to 50ml (tele-systolic volume: TSV) to 115 to 130ml (tele-diastolic volume: TDV). This distends the LV and increases pressure at its level (Figure 5). Ventricular diastolic pressure is thus of the order of 5mmHg (Figure 6). PAGE 3  Figure 5. Hemodynamic phenomena during the cardiac cycle (1) Figure 6. Left ventricular (LV) pressure-volume relationship ISOVOLUMETRIC CONTRACTION The ventricles contract to propel blood into the aorta and pulmonary artery. The sigmoid, mitral and tricuspid valves are closed as blood pressure in the ventricles closes them. The ventricles begin to contract at constant ventricular volume. Intra-GV pressure rises to ≥ Aortic pressure (Pr Ao) (80mmHg), inverting the Ao-GV and pulmonary artery (PA)-VD pressure gradient and opening the aortic and pulmonary sigmoid valves. (Figures 5 et 6). PAGE 4 VENTRICULAR EJECTION It begins with the opening of the sigmoid valves. It consists of 2 successive phases separated by the pressure peak. Ventricular contraction is strengthened, increasing intra-ventricular pressures to a peak of 120mmHg in the LV and 25mmHg in the VD.) This leads to rapid ejection (active following isotonic contraction of the ventricles), followed by slow ejection (passive). Ventricular volume decreases as blood is ejected from the ventricles. Systolic ejection volume (SEV) is around 70ml: SEV = SDV (115) - STV (45) = 70ml. Volume of blood ejected  50% of blood present in the ventricles at the end of diastole. Residual volume or telesystolic volume (TSV): the greater the force of contraction, the smaller the residual volume. It constitutes a reserve for increasing flow. Aortic valve closure occurs when LV Pressure < Ao Pressure (80mmHg) (Figures 5 et 6). ISOVOLUMETRIC RELAXATION The LV relaxes while the valves are closed, resulting in a rapid drop in intra-GV Pr = diastolic Pr ≈ 0mmHg and intra-GV blood volume equal to STV= 45- 50ml of blood.Closure of the sigmoid valves is caused in part by a small reflux of blood towards the ventricle giving a catacrote Incisure. Aortic pressure rebound is due to the elastic force of the aorta (reflecting the quality of aortic elasticity), giving a dicrotic wave. All in all: a pulsed circulation of ventricular origin gives rise to a straightened circulation in the aorta. Mitral atrial pressure rises as a result of venous return (v wave).this phase ends with the opening of the AV valves and a sudden drop in atrial pressure (y wave) (Figures 5 and 6).the pulmonary pressure curve is identical to the aortic pressure curve, but pressures are six times lower. (Figure 7). Figure 7. Pulmonary and right ventricular arterial pressures during the cardiac cycle PAGE 5 Cardiac pressures therefore vary during the cardiac cycle. (Table 2). Systole Diastole Moyenne OG Variable Variable 5- 12 (7) (0) VG 120 0 -12 Aorte 120 70 - 80 85 OD Variable Variable 4- 7 (+3) (-3) VD 20-25 0- 7 Artère 20-25 8-10 15 pulmonair e Table 2. Cardiac pressures during the cardiac cycle Heart sounds In clinical practice, heart sounds can be detected by auscultation with a stethoscope. It's important to remember that valve opening is not audible (it's a slow process that makes no sound), and that it's valve closure that produces the heart sounds audible through the stethoscope.Four heart sounds can be distinguished: 2 audible on auscultation: B1 « TOUM » et B2 « TAM » 2 non audible on auscultation: B3 and B4, can be detect by PHONOCARDIOGRAMME., The origins of these noises are: B1: A-V VALVE CLOSURE B2: SIGMOID VALVE CLOSURE B3: RAPID FILLING OF VENTRICLES B4: CONTRACTION OF THE ATRIA Audible heart sounds can be detected at heart auscultation sites (Figure 8). PAGE 6  Figure 8 : Focus of cardiac auscultation Note: Heart murmurs are abnormal heart sounds detected in cases of valve lesions (narrowing or insufficiency). Exemple : Aortic insufficiency (AIo), where the aortic valves are incontinent, results in blood reflux into the LV during diastole, giving rise to the diastolic murmur detected at the aortic focus. (Figure 9). Insufficient aortic valve Figure 9. Aortic insufficiency Cardiac work: Pressure-volume relationships during the cardiac cycle This is the work done by the heart with each beat. It corresponds to the amount of energy the heart converts into work each time it ejects blood into the arteries. PAGE 7 In biophysical terms, cardiac work (W), the myocardial energy expenditure, is the product of the pressure gradient (PD) and the volume gradient (VG). W=PDxVD PD=pressure difference VD=volume difference DP = Arterial Pressure (AP) - Venous Pressure = AP (since PV is negligible) DV = cardiac output (Qc), thus, Hence, Note : Cardiac output is only 5-10% under resting conditions, but increases to 15% during exercise. The heart has low energy reserves, but, unlike striated skeletal muscle, is highly flexible in its use of substrates. It can use free fatty acids, ketones and lactates. The ability to use lactate ensures that the heart functions well during prolonged intense physical effort. THE CONCEPTS OF "PRECHARGE" AND "POSTCHARGE Pre-load: this is the degree of muscular tension at the start of the contraction, which depends on the volume of blood in the LV at the end of diastole (VTD) and on ventricular filling (venous return). EDV: end diastolic volume Afterload: this is the load against which the muscle exerts its contractile force. It depends on the systolic pressure in the aorta. ESV: end systolic volume Stroke Volume (SV) FRANK-STARLING MECHANISM SV=EDV-ESV FRANK-STARLING's law states that: "The energy of contraction is proportional to the initial length of the cardiac muscle fiber". The more the cardiac muscle is stretched during filling (VTD), the greater its force of contraction (contractility or inotropism) and the greater the amount of blood ejected into the aorta (VES). Thus, VTD is a function of the length of the V myocardial muscle fibers: this is passive tension. ESV is a function of contraction force: this is active tension (Figure 10).cardiac cell length, which is determined by the extent of venous return, is normally less than optimal. The increase in venous return brings the cells closer to their optimal length, which in turn increases the force of contraction during systole, and hence the ESV (Figures 10 and 11). PAGE 8 Figure 10. Frank-Starling's law of the heart PRESSURE-VOLUME RELATIONSHIP DURING THE CARDIAC CYCLE (FIGURE 11) A relationship exists between VES (cardiac output) and preload or VTD. The mechanisms are: increased sarcomere length sensitizes troponin C to Ca2+and increases intracellular Ca2+availability, bringing actin and myosin filaments closer together and causing maximum acto-myosin bridging. Figure 11. Pressure-volume relationship of the heart's left ventricle PAGE 9 Thus, Frank-Starling's Law can be written as follows: "The energy of contraction (VES) is proportional to the initial length of the cardiac muscle fiber (VTD)". Cardiac output and its regulation DÉFINITIONS Cardiac output (Qc) is the amount of blood ejected by the ventricle per minute (l/min). This is a very important parameter, on which the irrigation of the body's various organs depends. It is regulated to adapt cardiac output to the body's needs. For an adult male (weight=70Kg, SC = 1.7m2) at physical and mental rest, Qc = 5 to 6 l/min, with VD Qc = VG Qc. We also define the cardiac index = cardiac output/body surface area = 2.5 to 4 l/min/m2 PHYSIOLOGIC VARIATIONS Cardiac output (Qc) increases in the digestive period (30%), at the end of pregnancy (40%), under stress (50-100%), during physical exercise (25-30 l/min). Qc decreases when moving from the supine to the upright position (-20 to -30%). It also varies according to the body's metabolic rate, age and size. At rest, Qc is distributed as follows in the body: Myocardium: 250 mL/min (5%), Skeletal Muscles: 850 mL/min (16%), Brain: 750 mL/min (15%), Skin: 450 mL/min (8%), Kidney: 1200 mL/min (22%), Hepato-Splanchnic Circulation: 1500 mL/min (28%), and the rest: 350 mL/min (6%). FACTORS DETERMINING CARDIAC OUTPUT The determining factors of Qc are heart rate (Fc), which depends on the autonomic nervous system, and systolic ejection volume (SEV), which depends on the pre-load, afterload and contractility of the cardiac muscle. Pre-load, which provides information on the degree of cardiac muscle tension at the start of contraction (Ventricular Filling = VTD), depends on venous return, which in turn depends on : - Sympathetic venous tone - Thoracic negative pressure - the cardiac pump: ventricular compliance - the muscular pump: skeletal striated muscle contraction (Figure 12). PAGE 10 Afterload: this is the load against which the muscle exerts its contractile force, and depends on Aortic Pressure (AP) and Aortic Resistance. As long as BP does not exceed 160mmHg, there is no drop in ESV and therefore cardiac output. Under normal conditions, with a BP between 80 and 140 mmHg, cardiac output does not depend on afterload, but only on preload (venous return). (Figure 13). Figure 13. Variations in cardiac output (Qc) as a function of blood pressure (BP) RÉGULATIONOF CARDIAC OUTPUT Qc regulation is an integrated action of intrinsic and extrinsic mechanisms. Regulation of cardiac output helps to regulate BP, blood volume and distribution in the body. Intrinsic regulation Intrinsic regulation is Frank Starling's Law = Law of the Heart. Indeed, any ↗venous return→ ↗ cardiac filling → ↗ cardiac muscle fiber length → ↗ VTD→ ↗ VES → ↗ Qc. Starling's Law ensures identical flow between the heart's R and L ventricles at all times. PAGE 11  Extrinsic Regulation 1) Nervous regulation: VNS (Figure 14) Figure 14. Nerve regulation of cardiac output:;CM: cardiomodulator, VM: vasomotor, PS: parasympathetic, S: sympathetic, R: receptor, M: muscarinic, NAD: noradrenaline, Ach: cetylcholine, X: nerve X the vagus - Role of the sympathetic system: essentially innervates the ventricles and hence the myocardium. It has a positive inotropic (I+) and positive chronotropic (C+) effect, increasing VES and Fc respectively, and consequently Qc (Figure 14). The neuromediators of this system are the catecholamines adrenaline (AD) and noradrenaline (NAD), whose receptors are β1-adrenergic coupled to a Gs protein. The second messenger is ↗ cAMP. (Figure 15). Figure 15. Role of the sympathetic nervous system in regulating cardiac output PAGE 12  Note : All substances that increase cAMP have an I+ effect: - Caffeine, theophylline: inhibit cAMP degradation - Glucagon: ↑ cAMP formation - Digitalis: digoxin: inhibit myocardial Na+/K+ ATPase pump →↑[Ca]int - Role of the parasympathetic system: it has a negative chronotropic (C-) and negative inotropic (I-) effect, resulting in a significant drop in Fc and a low VES (20 to 30%). Its neuromediator is acetylcholine (Ach), which acts on a muscarinic cardiac receptor (M2), and its second messenger is the decrease in cAMP. Note the weak parasympathetic innervation of the ventricles. It mainly innervates the two atria. I-acting substances that simulate parasympathetic action include hypercapnia, hypoxia, acidosis and beta-blockers.. D+ (Dromotropic Effect): 2) Hormonal Regulation -Refers to an increase in the conduction velocity of electrical - Catecholamines (AD and NAD): originating from the adrenal medulla, they impulses through the heart. have the following effects I+, C+ et D+ -Catecholamines increase the speed of action potential propagation, particularly through the atrioventricular - Thyroid hormones: by increasing myocardial Rβ adrenergic gene expression, the (AV) node, leading to more efficient coordination of atrial and ventricular effect of catecholamines is potentiated. contractions. Note Low cardiac output can be : - Of cardiac origin: MI, myocarditis, heart failure (cardiogenic shock) - Due to reduced venous return: Hypovolemia (hemorrhage), obstruction of large veins, acute venous vasodilatation (Circulatory shock). High cardiac output may be maintained in cases of : - Anemia: reduced blood viscosity - arterial VD: reduced afterload Cardiac output measurement FICK METHOD Fick's principle = the amount of substance taken up by an organ is equal to the arteriovenous difference in the concentration of that substance multiplied by the cardiac output. At heart level, the substance is oxygen (O2), the organ is the whole organism, the amount of substance taken up = V'O2 and the arterio-venous difference of O2 = Peripheral arterial O2 content (Cart) - Venous O2 content (Cv=Pulmonary Cart). (Figure 16). PAGE 13  Figure 16. Fick's principle So, Hence, With, Cart peripheral O2: measured by blood sampling from a peripheral artery (radial), Cart pulm O2 : Cveinous O2: measured by catheterization of the right heart and V'O2 : measured by spirometry. OTHER METHODS Echo-Doppler : C'est la méthode la plus simple et la plus utilisée en pratique médicale, mais moins précise car très variable. - Method for diluting an indicator - Radioactive dye or tracer: the most widely used is 131I-labeled plasma albumin. Qc = indicator quantity injected/average tracer concentration during the first passage through the heart. - Thermodilution: Performed using a Swan-Ganz catheter. A certain quantity of liquid (cold saline at room temperature or 0°C) is injected through the proximal site of the catheter. The change in temperature measured by the thermistor at the tip of the catheter (i.e., downstream of the injection site) is globally proportional to cardiac output. This is the reference method for hemodynamic exploration, but it is highly variable (depending in particular on injection speed), so it needs to be repeated several times and averaged. References 1. Arthur C. Guyton et John E. Hall. Précis de Physiologie Médicale. 2ème édition Française. PICCIN. 2003. 2. Hervé Guénard. Physiologie humaine. Editions Pradel. 4ème édition, 2009. 3. Marieb, Elaine N. Anatomie et physiologie humaines. Pearson Education France. 2005. 4. William F Ganong. Physiologie Médicale. Les presses de l'Université de Laval, 19ème édition, 2001 5. Sherwood L. Physiologie Humaine. 2ème édition Française. De Boeck. 2006 PAGE 14