dr. Sri Lestari Sulistyo Rini, MSc CARDIAC PUMP dr. Sri Lestari Sulistyo Rini, MSc

Phases of the Cardiac Cycle Figure 20–16

8 Steps in the Cardiac Cycle Atrial systole: atrial contraction begins right and left AV valves are open Atria eject blood into ventricles: filling ventricles Atrial systole ends: AV valves close ventricles contain maximum volume end-diastolic volume (EDV) Ventricular systole: isovolemic ventricular contraction pressure in ventricles rises AV valves shut

8 Steps in the Cardiac Cycle Ventricular ejection: semilunar valves open blood flows into pulmonary and aortic trunks Stroke volume (SV) = 60% of end-diastolic volume Ventricular pressure falls: semilunar valves close ventricles contain end-systolic volume (ESV), about 40% of end-diastolic volume

cardiac cycle

8 Steps in the Cardiac Cycle Ventricular diastole: ventricular pressure is higher than atrial pressure all heart valves are closed ventricles relax (isovolumetric relaxation) Atrial pressure is higher than ventricular pressure: AV valves open passive atrial filling passive ventricular filling cardiac cycle ends

3 Factors that Affect ESV Preload: ventricular stretching during diastole Contractility: force produced during contraction, at a given preload Afterload: tension the ventricle produces to open the semilunar valve and eject blood

1. Preload The degree of ventricular stretching during ventricular diastole Directly proportional to EDV Affects ability of muscle cells to produce tension

Frank-Starling Mechanism The amount of blood pumped by the heart is determined by the rate of blood flow from the veins (venous return). The intrinsic ability of the heart to adapt to increasing volumes of blood is the Frank-Starling mechanism. With the extra delivery of blood, the cardiac muscle contracts with greater force because of improved actin/myosin interaction.

Frank-Starling Mechanism Allows the heart to readily adapt to changes in venous return. The Frank-Starling Mechanism plays an important role in balancing the output of the 2 ventricles. In summary: Increasing venous return and ventricular preload leads to an increase in stroke volume.

Stroke Volume Cont., Preload The degree of ventricular stretch at end-diastole The Frank-Starling Law of the Heart  Preload =  Contractility (to a point) Factors Affecting Preload Circulating volume Body positioning Atrial systole Medications Diuretics (i.e. Lasix) ACE Inhibitors I.V. Fluids Starling Curve

Physical Limits Ventricular expansion is limited by: myocardial connective tissue the fibrous skeleton the pericardial sac End-Systolic Volume (ESV) The amount of blood that remains in the ventricle at the end of ventricular systole is the ESV

Factors Affecting Heart Rate and Stroke Volume Autonomic nervous system: sympathetic and parasympathetic Circulating hormones Venous return and stretch receptors Figure 20–24

2. Contractility The inherent capacity of the myocardium to contract independently of changes in afterload or preload. Changes in contractility are caused by intrinsic cellular mechanisms that regulate the interaction between actin and myosin independent of sarcomere length. Alternate name is inotropy.

Contractility Force of contraction Increased rate and/or quantity of Calcium delivered to myofilaments during contraction Heart functions at lower end-systolic volume and lower end-diastolic volume

Stroke Volume Cont., Contractility Positive inotropic agents  Force of contraction Negative inotropic agents  Force of contraction Factors that affect contractility Autonomic nervous system (ANS) Medications: Digoxin (Lanoxin) Beta-adrenergic blockers (i.e. metoprolol ) Calcium channel blockers (i.e. verapamil )

Contractility is affected by: autonomic activity & hormones : Sympathetic stimulation: NE released by postganglionic fibers of cardiac nerves epinephrine and NE released by adrenal medullae causes ventricles to contract with more force increases ejection fraction and decreases ESV Parasympathetic activity: acetylcholine released by vagus nerves reduces force of cardiac contractions

Hormones and Contractility Many hormones affect heart contraction Pharmaceutical drugs mimic hormone actions: stimulate or block beta receptors affect calcium ions e.g., calcium channel blockers

3. Afterload More precisely defined in terms of ventricular wall stress: LaPlace’s Law: Wall stress = Pr/h P = ventricular pressure R = ventricular radius h = wall thickness

Afterload is better defined in relation to ventricular wall stress LaPlace’s Law Wall Stress Wall Stress P r h

Afterload Is increased by any factor that restricts arterial blood flow As afterload increases, stroke volume decreases

Stroke Volume Cont., Afterload Resistance to ventricular ejection during systole Factors that affect afterload Outflow impedance Left side High systemic blood pressures (SVR) Aortic valve stenosis Right side High pulmonary blood pressures (PVR) Pulmonary valve stenosis Diameter of arterial vessels Blood characteristics Medications: ACE (angiotension converting enzyme) inhibitors

EDV, Preload, and Stroke Volume At rest: EDV is low myocardium stretches less stroke volume is low With exercise: EDV increases myocardium stretches more stroke volume increases As EDV increases, stroke volume increases

Factors Involved in Regulation of Cardiac Output

STROKE WORK Stroke work (SW) refers to the work done by the ventricle to eject a volume of blood (i.e., stroke volume) into the aorta.  Stroke work is sometimes used to assess ventricular function. Cardiac work is the product of stroke work and heart rate, which is the equivalent of the triple produce of stroke volume, mean aortic pressure and heart rate. Analyze the stroke work using Left Ventricular Pressure Volume Loop To generate a PV loop for the left ventricle, the left ventricular pressure (LVP) is plotted against left ventricular (LV) volume at multiple time points during a complete cardiac cycle. 

Work Output of the Heart Understand how the systolic and diastolic pressure curves are derived. By combining the end diastolic and systolic curves, the volume-pressure diagram can be defined. The area inside the VP diagram is the EW.

Ventricular Function Curve The dependancy of stroke volume on preload was described more than 100 years ago by Otto Frank and E.H. Starling and since then has been called the Frank-Starling mechanism. Using this relationship between preload and stroke volume or stroke work, a ventricular function curve can be consructed by plotting stroke work at various levels of preload.

Point 1 on the PV loop is the pressure and volume at the end of ventricular filling (diastole), and therefore represents the end-diastolic pressure and end-diastolic volume (EDV) for the ventricle. As the ventricle begins to contract isovolumetrically (phase b), the LVP increases but the LV volume remains the same, therefore resulting in a vertical line (all valves are closed). Once LVP exceeds aortic diastolic pressure, the aortic valve opens (point 2) and ejection (phase c) begins. When the aortic valve closes (point 3), ejection ceases and the ventricle relaxes isovolumetrically - that is, the LVP falls but the LV volume remains unchanged, therefore the line is vertical (all valves are closed). The LV volume at this time is the end-systolic (i.e., residual) volume (ESV). When the LVP falls below left atrial pressure, the mitral valve opens (point 4) and the ventricle begins to fill. The width of the loop represents the difference between EDV and ESV, which is by definition the stroke volume (SV). The area within the loop is the ventricular stroke work.

Left Ventricular Pressure Volume Loop 120 Left Ventricular Pressure (mmHg) SV 6 ESV EDV 70 130 Volume (ml)

Left Ventricular Pressure Effects of an Increase in Preload on Left Ventricular Pressure Volume Loop Ejection Pressure 120 Left Ventricular Pressure (mmHg) SV EDV 6 70 130 Volume (ml)

VENTRICULAR COMPLIANCE As the ventricle fills with blood, the pressure and volume that result from filling are determined by the compliance of the ventricle. Is determined by the physical properties of the cardiac muscle and other tissues making up the ventricular wall as well as by the state of ventricular contraction and relaxation.

VENTRICULAR COMPLIANCE in ventricular hypertrophy the ventricular compliance is decreased ventricular end-diastolic pressure (EDP) is higher at any given end-diastolic volume (EDV) (see Figure). in some forms of heart failure, ventricular relaxation is impaired at a given EDP, a less compliant ventricle would have a smaller EDV

In a disease state such as dilated cardiomyopathy, the ventricle becomes very dilated without appreciable thickening of the wall. This dilated ventricle will have increased compliance as shown in the figure; therefore, although the EDV may be very high, the EDP may not be greatly elevated.

VENTRICULAR COMPLIANCE

PRELOAD EFFECTS

Left Ventricular Pressure Effects of an Increase in Afterload on Left Ventricular Pressure Volume Loop Left Ventricular Pressure (mmHg) 120 d SV 6 40 140 Volume (ml)

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