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diastolic dysfunction
- 1. Diastolic function of the heart, Phases, Enddiastolic volume & pressure, Factors affecting
- 2. Diastole • time period during which the myocardium loses its ability to generate force and shorten and returns to an unstressed length and force • Begins with the closure of aortic/pulmonic valves • 2/3rd of cardiac cycle • Total duration : 0.53 sec at HR of 72/min • Active & passive components
- 3. Active Relaxation • occurs in a series of energy- consuming steps • Release of calcium from troponin C, • detachment of the actin-myosin cross-bridge, • phosphorylation of phospholamban, • Sarcoplasmic reticulum calcium ATPase–induced calcium sequestration into the sarcoplasmic reticulum, • sodium/calcium exchanger– induced extrusion of calcium from the cytoplasm, • extension of the sarcomere to its rest length P m t m . c s ( p b e S r u s g a r a e f t
- 4. Phases of diastole • Protodiastole • Isovolumic relaxation • Rapid filling • Diastasis • Atrial kick
- 5. • The isovolumic relaxation phase is energy dependent • does not contribute to ventricular filling • Auxotonic relaxation phases (phases 2 through 4), ventricular filling occurs against pressure gradient (passive) • Encompasses a period during which the myocardium is unable to generate force and filling of the ventricular chambers takes place
- 6. Protodiastole – Once the ventricular muscle is fully contracted, the already falling ventricular pressures drop more rapidly – 0.04sec – ends when the momentum of the ejected blood is overcome and the aortic and pulmonary valves close
- 7. Isovolumic relaxation – from closure of the aortic valve to opening of the mitral valve – 0.03-0.06sec – Energy dependent – Left ventricular volume constant (no filling) – left ventricular pressure decreases
- 8. Rapid filling stage – Starts with opening of mitral valve – transmitral pressure gradient drives LV filling – 70-80% of filling – Early filling correlates with the E-wave of transmitral flow doppler
- 9. Diastasis – period of low flow in mid-diastole – Lt.Atrial Pressure=Lt.Ventricular Pressure – Little oR NO flow <5% – correlates with the interval between E- and the A-wave of the transmitral Doppler signal
- 10. Atrial kick – Atrial contraction leads to late rapid filling – Contributes 15-25% of LVEDV – correlates with the A-wave of the mitral inflow signal – Becomes important in AF, high ventricular rate, stiff ventricle
- 11. Diastolic time
- 12. Factors affecting diastolic function • passive chamber stiffness (remodelling) • elastic recoil of the ventricle • the diastolic interaction between the two ventricular chambers • systolic volume load • atrial properties (rhythm,contractn) • Drugs (catecholamines)
- 13. Effects of beta stimulation • Increases both ionotropy and lusitropy (relaxation) • Ionotropic state regulated by Ca concentration in cytoplasm, increased by beta stimulation (cAMP mediated) • Lusitropy governed by phosphorylation of phospholamban and Troponin I, which is partially regulated by beta stimulation.
- 15. Invasive assessment • Done by measurement of LV pressure with a high-fidelity micromanometer catheter • Calculates the peak instantaneous rate of LV pressure decline, peak dP/dt, and the time constant
- 16. Non-invasive Assessment Via Doppler echocardiography Flow velocities are measured across the mitral valve during diastole
- 19. End Diastolic Volume (EDV) Volume at the end of diastole (end of ventricular filling). In a healthy heart this is directly proportional to venous return End Systolic Volume (ESV) Volume at the end of systole end of ventricular contraction Stroke Volume (SV) = EDV - ESV Ejection Fraction (EF) = SV/EDV Left Ventricular Volumes - Definitions Left ventricular norm for EF at Rest: approximately 62% Left Ventricular norms for Max Exercise: approximately 80%
- 20. End-diastolic volume • Normally 110-120 ml can increase to 180 ml
- 21. Preload • The initial length of the cardiac muscle fibre before contraction begins • can be equated to the end-diastolic volume • Clinically equated to the CVP when studying the RV or the PAOP when studying the LV
- 22. Starlings Law of the Heart and Contractility SV (left ventricular performance) Preload (venous return or EDV) u Contractility Normal Contractility d Contractility (heart failure) Preload X SV at Preload X - u contractility SV at Preload X – Normal cont. SV at Preload X - d contractility Starling’s Law: The greater the EDV (blood going in the heart), the more blood comes out of the heart The State of Myocardial Contractility determines the amount of blood (SV) that comes out of the heart at a given preload
- 23. Factors affecting preload • Venous return • Blood volume • Posture • Intra-thoracic pressure • Pericardial pressure • Venous tone • Heart rate & rhythm
- 25. Left Ventricular Pressure (mmHg) Volume (ml) Aortic Valve Closes ESV ESP Mitral Valve Closes EDV EDP Mitral Valve Opens Ventricular Filling Begins Aortic Valve Opens 120 6 40 140 Left Ventricular Pressure Volume Loop Isovolumic contraction SV Slope of dashed line: ventricular contractility
- 26. Left Ventricular Pressure (mmHg) Volume (ml) 120 6 40 140 Effects of an Increase in Preload on Left Ventricular Pressure Volume Loop u EDV u EDP u Ejection Pressure u SV
- 27. Left Ventricular Pressure (mmHg) Volume (ml) 120 6 40 140 Effects of an Increase in Afterload on Left Ventricular Pressure Volume Loop u ESV u ESP d SV
- 29. Diastolic heart failure • Heart failure accompanied by predominant or isolated abnormality in diastolic function, this clinical syndrome is called. • symptoms and signs of heart failure, a preserved ejection fraction (EF), and abnormal diastolic function
- 30. Diastolic failure • predominantly occurs in patients over the age of 65 and • for unclear reasons is more common in women • Hypertension the most common underlying etiology. Other risk factors include diabetes mellitus, obesity, and bilateral renal artery stenosis
- 31. • Diastolic failure may also appear in elderly patients without any known predisposing • factors, possibly as an exaggeration of the normal stiffening of the heart with age,
- 32. Diastolic failure criteria • European society of cardiology 1. Signs/symptoms of CHF 2. Normal ?EF 3. Evidence of abnormal LV relaxation,filling,distensibility or stiffness
- 33. Left ventricular hypertrophy with and without dilation, viewed in transverse heart sections. Compared with a normal heart (center), the pressure-hypertrophied hearts (left) have increased mass and a thick left ventricular wall, while the hypertrophied, dilated heart (right) has increased mass and a normal wall thickness normal pressure-hypertrophied Volume hypertrophied,dilated
- 35. • Textbook of physiology Guyton & Hall • Ganong’s review of med. Physiology • Miller’s anesthesia 7th edn • Clinical anesthesiology Morgan & mikhail • http://123sonography.com/node/939 • http://circ.ahajournals.org/content/105/11/1387 .full • http://www.aafp.org/afp/2006/0301/p841.html
Notas do Editor
- Important since coronary flow occurs during diastole
- Relaxation occurs in a series of energy-consuming steps beginning with the release of calcium from troponin C, detachment of the actin-myosin cross-bridge, phosphorylation of phospholamban, sarcoplasmic reticulum calcium ATPase–induced calcium sequestration into the sarcoplasmic reticulum, sodium/calcium exchanger–induced extrusion of calcium from the cytoplasm, slowing of cross-bridge cycling rate, and extension of the sarcomere to its rest length
- Relaxation(meaning the active phase,isovolumic relaxn) occurs in a series of energy-consuming steps beginning with the release of calcium from troponin C, detachment of the actin-myosin cross-bridge, phosphorylation of phospholamban, sarcoplasmic reticulum calcium ATPase–induced calcium sequestration into the sarcoplasmic reticulum, sodium/calcium exchanger– induced extrusion of calcium from the cytoplasm, slowing of cross-bridge cycling rate, and extension of the sarcomere to its rest length
- The isovolumic relaxation phase is energy dependent. During the auxotonic relaxation phases (phases 2 through 4), ventricular filling occurs against pressure. It encompasses a period during which the myocardium is unable to generate force and filling of the ventricular chambers takes place. The isovolumic relaxation phase does not contribute to ventricular filling. Miller’s anesthesia
- During the auxotonic relaxation phases (phases 2 through 4), ventricular filling occurs against pressure. It encompasses a period during which the myocardium is unable to generate force and filling of the ventricular chambers takes place.
- Once the ventricular muscle is fully contracted, the already falling ventricular pressures drop more rapidly
- The left atrium is filled while the left ventricle is in a state of relaxation. The pressure gradient is rather small, but still sufficient to open the mitral valve and permit filling. A second important factor of early filling is diastolic recoil of the ventricle. Especially in young and healthy individuals this recoil causes suction, which drags blood from the atria into the ventricle. Filling of the ventricle is also caused by the motion of the heart itself. During diastole the ventricle expands and engulfs the volume of the left atrium. Early filling correlates with the E-wave of transmitral flow. Basically, the size and velocity-time integral of the E-wave reflect the quantity of blood that enters the ventricle during early filling
- Filling of the ventricle causes pressure in the left ventricle to rise. When equilibration of pressure between the atrium and the ventricle occurs, transmitral flow ends and the mitral valve partially closes. This phase, during which little or no filling occurs, is known as diastasis and correlates with the interval between the E- and the A-wave of the transmitral Doppler signal. http://123sonography.com/node/939
- Exercise and ventricular filling=Increased heart rate cuts down time spent in diastole. To compensate, the ventricles actively relax and create a suction effect that draws more blood into ventricles
- Many different factors influence diastolic function: systolic volume load, passive chamber stiffness, elastic recoil of the ventricle, the diastolic interaction between the two ventricular chambers, atrial properties, and catecholamines. Whereas systolic dysfunction is a reduced ability of the heart to eject, diastolic dysfunction is a decreased ability of the heart to fill. Miller’s anesthesia
- http://www.flashcardmachine.com/25cardiac-diastolic-function.html
- Isovolumic relaxation can be quantified by measurement of LV pressure with a high-fidelity micromanometer catheter and calculation of the peak instantaneous rate of LV pressure decline, peak (−) dP/dt, and the time constant of isovolumic LV pressure decline
- The auxotonic LV filling phases of diastole can be characterized by Doppler echocardiography or by radionuclide, conductance, or MRI techniques. Whereas each technique has advantages and disadvantages, all assess diastolic function by measuring indices of volume transients during ventricular filling
- degree of tension on the muscle when it begins to contract, which is called the preload. For cardiac contraction, the preload is usually considered to be the end-diastolic pressure when the ventricle has become filled.
- NOTE: Resting Ejection Fraction (EF) is the best indicator of both heart performance and heart disease prognosis
- Preload - The initial length of the cardiac muscle fibre before contraction begins. This can be equated to the end-diastolic volume and is described by the Frank–Starling mechanism. Clinically it is equated to the CVP when studying the RV or the PAOP when studying the LV.
- Preload - The initial length of the cardiac muscle fibre before contraction begins. This can be equated to the end-diastolic volume and is described by the Frank–Starling mechanism. Clinically it is equated to the CVP when studying the RV or the PAOP when studying the LV.
- Frank–Starling law -The strength of cardiac contraction is dependent upon the initial fibre length.
- ?PEEP as well?
- When heart failure is accompanied by a predominant or isolated abnormality in diastolic function, this clinical syndrome is called diastolic heart failure. symptoms and signs of heart failure, a preserved ejection fraction (EF), and abnormal diastolic function
- Robbins 8th edition
- Normal EF > 50%
- The pattern of hypertrophy reflects the nature of the stimulus. In response to increases in pressure (e.g., hypertension or aortic stenosis), ventricles develop pressure-overload hypertrophy , which usually causes a concentric increase in wall thickness. In pressure overload, new sarcomeres are predominantly assembled in parallel to the long axes of cells, expanding the cross-sectional area of myocytes. In contrast, volume-overload hypertrophy is characterized by ventricular dilation. This is because the new sarcomeres assembled in response to volume overload are largely positioned in series with existing sacromeres. As a result, in dilation due to volume overload the wall thickness may be increased, normal, or less than normal; thus, heart weight, rather than wall thickness, is the best measure of hypertophy in volume overloaded hearts. Robbin’s pathology 8th edition
- At a functional level, cardiac hypertrophy is associated with heightened metabolic demands due to increases in wall tension, heart rate, and contractility (inotropic state, or force of contraction), all of which increase cardiac oxygen consumption. As a result of these changes, the hypertrophied heart is vulnerable to decompensation, which can evolve to cardiac failure and eventually lead to death.