* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Download Cardiac Function Curve
Survey
Document related concepts
Electrocardiography wikipedia , lookup
Coronary artery disease wikipedia , lookup
Cardiac contractility modulation wikipedia , lookup
Heart failure wikipedia , lookup
Myocardial infarction wikipedia , lookup
Cardiac surgery wikipedia , lookup
Aortic stenosis wikipedia , lookup
Lutembacher's syndrome wikipedia , lookup
Hypertrophic cardiomyopathy wikipedia , lookup
Mitral insufficiency wikipedia , lookup
Antihypertensive drug wikipedia , lookup
Arrhythmogenic right ventricular dysplasia wikipedia , lookup
Dextro-Transposition of the great arteries wikipedia , lookup
Transcript
Cardiac Function Curve Clive M. Baumgarten, Ph.D. OBJECTIVES: 1. Describe the cardiac function curve (CFC) 2. Describe he relationships between (a) length and volume and (b) tension and pressure 3. Identify diastolic and systolic pressure-volume curves 4. Construct a pressure-volume loop and describe the determinants of stroke volume 5. Describe heterometric compensation for changes in afterload and contractility 6. Generate the CFC from changes in right atrial pressure 7. Describe the factors that modulate the CFC I. DEFINITIONS A. Systole: Active contraction of the heart. About 1/3 of the cardiac cycle. B. Diastole: Relaxation and refilling of chambers. C. Heart Rate (HR): Number of contractions per minute (beats/min). D. Stroke Volume (SV): Amount of blood ejected during systole (ml/beat) SV = EDV - ESV 1. End Diastolic Volume (EDV): Volume of blood in ventricle the instant before systole begins. 2. End Systolic Volume (ESV): Volume of blood in ventricle at completion of systole as marked by closure of the aortic and pulmonic valves. 3. Ejection Fraction = SV/EDV ≥ 0.55 E. Cardiac Output (CO) = SV X HR SV typically is 1 ml/kg. For a 70 kg individual 70 ml/beat × 72 beats/min = 5,040 ml/min ≈ 5 liters/min F. Cardiac Index (CI) = CO/body surface area CI = 2.2 - 4.0 L/min/m2 II. CARDIAC FUNCTION CURVE The cardiac function curve relates right atrial pressure (RAP or PRA), the factor controlling blood flow into the heart, to cardiac output, the blood flow from the heart. The basis for the curve is essentially a transformation of 1-dimensional lengthtension relationships into 3-dimensions. A change in length gives a change in volume, and tension gives pressure. A. 1-D to 3-D transformation: assuming heart is a thin-walled sphere. 1-Dimension 3-Dimensions Transformation ____________________________________________________________________________ Length (L) Volume (V) V = 4/3πr 3 ; C = 2πr = 4/3π(C/2π) 3 3 V∝C ____________________________________________________________________________ Tension (T) Pressure (P) P = 2HT/r ____________________________________________________________________________ r = radius C = circumference H = wall thickness 1. Geometry causes amplification of length changes: volume α (length)3 2. Law of Laplace relates tension and pressure. Remember that tension controls sarcomere length. P = 2HT / r Tension and, therefore, sarcomere length is related to P, r and H T P T r T 1/H B. A more accurate representation of the heart is as an ellipsoid: V = 4/3 × (Dap/2)(Dlat/2)(Dmax/2) III. STROKE VOLUME A. Determinants of End Diastolic Volume. Atrial pressure is the preload on the intact heart. During diastole Patrial is initially greater than Pvent. Blood flows into the ventricle until the pressures are equal (ignoring the inertia of blood). The volume contained at this time is EDV; the pressure is end diastolic pressure (EDP). The relationship between diastolic pressure and diastolic volume is the Ventricular Diastolic Pressure Curve. B. Determinants of End Systolic Volume. Arterial (aortic) pressure is the afterload on the intact heart. Fiber shortening and ejection of blood cannot occur until intraventricular pressure just exceeds aortic pressure. For the right ventricle, pulmonary artery pressure is the afterload. Diastolic pressure in left ventricle is greater than that in right ventricle. C. Isovolumetric (Isometric) Systolic Pressure Curve Relates maximum isovolumetric developed pressure to EDV. To obtain the curve, the aorta is cross-clamped to prevent injection of blood and fiber shortening. Upon excitation, the contraction is isovolumetric; pressure increases from its diastolic value, set by EDV and EDP, to a maximum pressure. Connecting the maximum isovolumetric developed pressures obtained at different EDV gives the isovolumetric systolic P-V curve. This relationship also is known as Starling's Law of the Heart or the Frank-Starling relationship. We usually use the curves for the left heart, but analogous curves can be drawn for the right heart. Therefore, scales for both right and left atrial pressure are shown. D. Pressure-Volume Loop A cycle of contraction, ejection, relaxation and refilling is termed a pressurevolume loop. Combining the diastolic and systolic curves, allows determination of SV (i.e., the amount of shortening) as a function of preload (EDV), afterload (aortic pressure), and contractility. These curves represent changes in only one variable while the others are held constant. Physiologically, changes in one variable often cause a change in a second. 1. Effect of preload. Initially (A), the left atrial pressure (~5 mm Hg) sets EDV (140 ml). Upon excitation, the heart contracts isovolumetrically until (B), when the aortic valve opens. Ejection of blood occurs, and ventricular volume falls (B − C). Note, ventricular pressure is not really constant during ejection because of the compliance of the aorta and the differing rates of blood flow into and out of the aorta with time. At (C), the aortic valve closes (ESP, ESV), and the ventricle relaxes isovolumetrically (C to D). Intraventricular pressure (D) is now less than atrial pressure and filling begins (D to A). If EDV is increased (A'), SV also increases (assume constant Paortic). 2. Similarly, the effect of changes in afterload and contractility on SV can be determined from pressure-volume loops. 3. SV depends on: • • Preload (EDV or PRA) ↑ preload → ↑ SV and ↓ preload → ↓ SV Afterload (Paortic) ↑ afterload → ↓ SV and ↓ afterload → ↑ SV $ Contractility ↑ contractility → ↑ SV and ↓ contractility → ↓ SV E. Heterometric (Frank-Starling) Compensation Pressure-volume loops and venous return combine to compensate for changes in SV and help maintain CO. Compensation implies a return of SV towards "normal" in response to a change in EDV, afterload or contractility. The basis for compensation is a shift of blood volume (BV) between arterial and venous circulation. Compensation operates over several beats and is incomplete. (Because compensation is incomplete, physiologically HR is reflexively adjusted to maintain CO and blood pressure.) IV. CARDIAC FUNCTION CURVE The cardiac function curve describes relationship between a right heart (input) parameter (RAP) and a left heart (output) parameter (CO). To isolate effects of RAP on CO, contractility, total peripheral resistance, and HR are held constant. In contrast, afterload (aortic pressure) is allowed to vary as a function of flow (CO). A. Linkage of right and left heart parameters follows from the series organization of the system. Flow from the right ventricle (QR) is a function of RAP described by a pressure-volume loop for the right heart. In turn, LAP is a function of QR. Finally, LAP is a determinant of QL, i.e., CO. B. To obtain the CFC, right atrium is attached to an infinite reservoir. The reservoir height controls RAP. RAP is set to different values, and CO is determined at each. At a constant HR, CO is a proportional to SV. Each pressure-volume loop (see diagram) corresponds to a different RAP. Note, because TPR is held constant, increased SV causes increased aortic pressure: Flow = ΔP/TPR . Typical Values of P-V Loops (from previous Figure) for Constructing CFC Graph: P-V Loops RAP EDV ESV SV __________________________________________________________________ I II III IV 0 4 7 10 140 240 335 510 60 100 160 335 80 140 175 175 __________________________________________________________________ Steepest part of cardiac function curve is between RAP = 0 and 4 mm Hg; at RAP ≥7 mm Hg, the CO reaches a plateau. C. CO when RAP < 0. When RAP < 0, one might expect no flow into right atrium and, consequently, a CO of 0. But, transmural pressure (PTrans = PIn - Pout) must be considered. For practical purposes, the heart sits in the intrapleural space, which has a negative pressure (about −4 mm Hg);. Note, pressures are measured relative to atmospheric pressure (0 mm Hg). Thus, if RAP = −1, then PIn = −1 and PTrans = (−1) − (−4) = +3. Thus, heart will expand and fill with blood. D. Plateau of Cardiac Function Curve. Several factors tend to limit CO as RAP increases. 1. Increasing afterload − Increased afterload offsets increased preload (See table above; compare EDV and SV at RAP of 7 and 10 mm Hg.) • As SV increases at a constant TPR, aortic pressure (afterload) increases. FLOW = ΔP/TPR The increase in afterload tends to limit SV. • The force-velocity relationship indicates that at high EDV, ejection of blood is faster than at low EDV. With faster ejection of blood, Paortic increases. 2. Pericardium − The pericardium is inelastic and limits EDV. IV. MODULATION OF CARDIAC FUNCTION CURVE A. Contractility: $ ↑ contractility (positive inotropic intervention) → ↑ SV and ↑ CO. $ ↓ contractility (negative inotropic intervention) → ↓ SV and ↓ CO. B. Total peripheral resistance: $ TPR → ↑ Paortic → ↓ SV and ↓ CO $ TPR → ↓ Paortic → ↑ SV and ↑ CO C. HR: At a constant SV, an increase in HR must increase CO. At HR > 100 bpm, diastole is too brief for complete filling, and EDV is reduced. HR × SV peaks at ~125 bpm under the conditions used to obtain the cardiac function curve. Increases in contractility and vascular compensation can give increases in CO up to HR of ~175 bpm in a healthy and fit patient. D. Atrial contraction. During tachycardia, atrial contraction ("atrial kick") makes an important contribution to ventricular filling (up to 20%). At the resting HR, however, atrial contraction has only a minor effect on EDV (5%). E. The time for diastolic filling of ventricle is inversely proportional to HR. At HR ≤100 bpm, filling is complete. At HR > 100 bpm, filling is incomplete, and if TPR and contractility are constant, CO falls at HR > 125 bpm. F. Effect of Heart Rate on Cardiac Output and Stroke Volume 1. Curve 1 makes the unphysiologic assumption that SV is independent of HR, and therefore, CO is directly proportional to HR. 2. Curve 2 considers only the effect of ventricular filling time on SV and CO. At HR > 125/min, CO falls. 3. Curve 3 considers the intact system and includes physiologic responses normally seen at elevated HR (increased contractility and decreased TPR). V. REFERENCES A. Koeppen, B.M. and Stanton, B.A. Berne & Levy Physiology, 6th Ed., 2008. pp 325-328, 376-380. B. Costanzo, L.S. Physiology, 3rd Ed., Saunders, 2006. Chapter 4, pp. 141-146. 3-cardiac function curve-2009.doc 8/28/2008