KN 252 Lecture 8: Cardiac Cycle Regulation – How blood is pumped

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KN 252
Marone Jane, Michael Jones

Cardiac Cycle Regulation – How blood is pumped The heart uses 3 principles in order to move blood through itself and the circulatory system: Pressure/flow – all things flow from high pressure to low pressure (where the heart accumulates high pressure, it will flow to an area of lower pressure) Elasticity – it is stretchable; its shape/volume will change depending on the relative pressure of material inside the heart versus that which is outside the heart (more stretch = more recoil) Mass balance – what goes in must come out; as blood enters the heart it will soon leave the heart through the great vessels Cardiac Cycle: Systole and Diastole Systole – period when the heart muscle contraction; creates high pressure in chamber Diastole – period when the heart muscle relaxes; drops pressure in chamber DIASTOLE (low pressure environment) 1. Atrial Diastole (atrial filling) – chamber stretches as blood fills (occurs before Ven. Dia) 2. Ventricular Diastole (ventricle filling) – chamber stretches as blood fills I. Isovolumetric Relaxation: period of time when ventricular pressure begins to drop, the pressure of blood from great vessels push down/closes SL valve ∗ Valves: AV not yet open; SL closed ∗ Volume: atrial = filling; ventricles = low II. Ventricular Filling: blood starts accumulating in atria which will drain into ventricle ∗ Valves: AV open; SL closed ∗ Volume: atrial = decreasing; ventricles = increasing SYSTOLE (high pressure environment) 1. Atrial Systole – occurs when atria contract; chamber becomes small (and pressure increases) as contraction occurs 2. Ventricular Systole – occurs when ventricles contract; chamber becomes small (and pressure increases) as contraction occurs; happens in two phases: I. Isovolumetric Contraction: period of time when pressure is increasing but volume remains constant (very beginning of ventricular systole) ∗ Valves: Atrioventricular valve is closed; semilunar valve not yet open ∗ Volume: constant II. Ventricular Ejection: pressure has built up to open SL valves; blood is now able to enter great vessels ∗ Valves: Atrioventricular valve is closed; Semilunar valve is open ∗ Volume: atrial = low; ventricles = high ***Once systole has completed the heart returns to ventricle diastole *** Pressure Differentials As the heart passes through the cardiac cycle, different pressures are generated 1. Left Atrium ranges from 0-12 mmHg; Right Atrium ranges from 0-6 mmHg 2. Left Ventricle ranges from 7-130 mmHg; Right Ventricle ranges from 4-24mmHg 3. Pulmonary Trunk ranges from 8-25 mmHg 4. Aorta ranges from 80-120 mmHg 5. Vena Cavae are around 0 Pulse Pressure = Systolic – Diastolic Heart Sounds pressure LUB = AV’s close; bicuspid closes before EX: Left Ventricle: 130-7 = 123mmHg tricuspid (pulse pressure) DUB = SLV’s close; aortic closes before EX: Right Ventricle: 24-4 = 20 mmHg pulmonary (pulse pressure) Cardiac Output Measure of heart function (greater CO = more efficient); amount of blood pumped out of each ventricle per minute Cardiac Output = Heart Rate x Stroke Volume EX: 75 bpm x 70 ml/beat = 5250 ml/min = 5.25 L/min Stroke Volume = End Diastolic Volume – End Systolic Volume EX: 120 ml – 50 ml = 70 ml Factors that influence Stoke Volume: o Preload – end diastolic volume (the amount of wall stretch that occurs in the ventricle as it completes diastole; completes filling) o Venous return – the more blood that flows in from the vena cavae into the heart the greater the preload/ the greater the volume • Muscle pump can influence an increase in venous return (exercising while cause more blood to be returned) • Respiratory pump can help draw blood into thorax increasing blood return (inspiration) Relationship between Preload and Stroke Volume: Starling’s Law: the greater the stretch, the greater the contraction Contractility – important for Cardiac Output The actual strength of a given contraction – related to the amount of calcium found in the sarcomere of each cardiac cell Positive Inotropism – chemical capable of increasing Negative Inotropism – chemical capable of decreasing contractility
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