* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Download Pressure – Volume Relationships
Survey
Document related concepts
Coronary artery disease wikipedia , lookup
Electrocardiography wikipedia , lookup
Artificial heart valve wikipedia , lookup
Cardiac surgery wikipedia , lookup
Cardiac contractility modulation wikipedia , lookup
Heart failure wikipedia , lookup
Myocardial infarction wikipedia , lookup
Antihypertensive drug wikipedia , lookup
Jatene procedure wikipedia , lookup
Hypertrophic cardiomyopathy wikipedia , lookup
Dextro-Transposition of the great arteries wikipedia , lookup
Mitral insufficiency wikipedia , lookup
Arrhythmogenic right ventricular dysplasia wikipedia , lookup
Transcript
Pressure – Volume Relationships Richard P. Wyeth Ph.D Gentleman’s Review Daniel Martingano OMS I Case Study • A 22 YO male athlete sees his team physician for his pre-season physical. During examination the physician notices a spitting of the second heart sound during deep inspiration. The most likely mechanism for this splitting is: A. Delayed closure of aortic valve B. Delayed closure of pulmonic valve C. Delayed opening of mitral valve D. Delayed opening of pulmonic valve Frank Starling Curve Right Ventricular v. Left Ventricular Systole • Peak systolic pressure of the RV is 4 to 5 x less than that of the LV • RV pumps like a bellows • LV forcefully from apex to base with slight cc twist • Duration of systole are approximately equal • Isovolumetric phase of loops represent longer time required to match afterload of Ao vs PA Right v. Left Pressure/Volume Relationships • Greater LV pressure alter phasic wave form compared to RV • Volumes moved are equal • LV/RV volume mismatches are resolved continuously Left Ventricular PV Loop as an Example • • • • • • With opening of mitral valve LV begins to fill passively (A) At B, LV diastolic pressure is lowest. Rapid filling in AB due to high LV compliance (DP/DP) Towards conclusion of BC atrial systole adds ~ 20% to diastolic volume as it stretches LV C is LVEDV/LVEDP. CD is isovolumetric contraction At D LV and Ao pressures equilibrate and Ao valve opens Rapid ejection occurs in DE Left Ventricular PV Loop as an Example • LV peak systolic pressure is developed at E • During EF LV systolic pressure and volumes decline • At F LV and Ao pressures again equilibrate and Ao valve closes • Isovolumetric relaxation occurs as LV pressures rapidly drop. FA • A represents end systolic volume unchanged from F • Cycle is complete Pressure Volume Loop Modulations and Stroke Volumes A. Increased preload increases LVEDV not LVESV — SV increases B. Increased afterload increases LVESV. LVEDV unchanged — SV decreases C. Increased contractility, a positive inotropic effect decreases LVESV not pressure — SV increases Resistance to Venous Return • Resistance to VR causes venous distention • Veins highly distensible (vessels of capacitance not resistance) Little change in venous pressure • Arteries have little capacitance and contribute ~1/3 of resistance • Veins contribute ~2/3 of resistance to VR – Capillaries separate arterial from venous side – Resistance is from venule to right atrium or left Venous Return Determines Central Venous Pressure • As VR increases RAP decreases (I) • As RAP increases VR decreases (II) • CVP = RAP • As VR increases CVP decreases • As CVP increases VR decreases • When VR = 0 RAP = MSFP Matching CO with VR • As VR increases – CO increases • As VR decreases – CO decreases Matching CO with VR Effects – Increasing Volume • Increasing volume (“Transfusion") shifts the vascular function curve to the right (Return to RA) – A match between the cardiac output and venous return now occurs at a higher RAP with an increased CO Matching CO with VR Effects – Contractility & Vascular Resistance • • Increasing cardiac contractility (positive inotropic effect) shifts cardiac function curve upward Increasing Vascular resistance (total peripheral resistance ) shifts both CO and VR downward Matching CO with VR Effects – Increasing Volume, Contractility, & Vascular Resistance • • • • What must be done CO to raise with increased resistance? – Increase inotropy Will increased resistance increase afterload? – Yes it will take more static work to open aortic valve (pulmonary valve also) Is this a good or bad thing? What about the converse? – decrease in resistance Venous v. Arterial Volume Distribution & MSFP • Total blood volume is sum of venous and arterial volumes – Venous is unstressed (D in volume will not change MSFP) – Arterial is stressed and will change MSFP Venous v. Arterial Volume Distribution & MSFP • Notice here that changes in venous volume must be greater than 4 L to affect increases in MSFP. • This also shows that little arterial blood will be found in adult volumes < 4L. – What does that tell you about hypovolemia and hypotension? • What about blood redistribution? – Decreased venous compliance vs increased. Measuring Contractility – Systolic Performance •Maximum “dp/dt” is maximal rate of pressure change per time change • Most accurate measure of in vivo ventricular systolic performance dpdt LV •Measured during isovolumetric contraction – independent of pre- and afterload Heart Performance Summary Heart performance is interrelated: – Related to Frank Starling Relationship – Autonomic Status – Preload increases increase performance – Afterload increases decrease performance – Contractility is independent of pre- and afterload – Frequency, increased HR preload decreases SV decreases. Decreased HR preload increases SV increases Cardiac Power Output • CPO is a measure of overall heart function incorporating flow and pressure generating capacities. – Good indication of maximun contractile force of heart. • Determining CO at rest and at VO2max allows you to determine Cardiac Reserve (CR). • Normal (untrained) 1 W at rest …12 W at maximum exercise (VO2 max ) – Normally patients have a 3 W or better CR. – Less has been shown as a predictor of increased mortality. Heart Failure – Cardiac Cycle Inadequacy • In failure heart can not compensate for increasing perfusion demands (exercise) by increasing cardiac output. • Not only are there left and right failures, there are diastolic and systolic failures – Weak muscle characterizes systolic (contractility) failures – Stiff muscles characterize diastolic (preload) failures Heart Failure – Cardiac Cycle Inadequacy • Heart failure is the inability of the heart to pump sufficient blood to maintain normal exercise. – The greater the failure the lesser the cardiac reserve. • Clinically, cardiac reserve can be approximated by determining cardiac output power at rest and at VO2 max. – Most clinical presentations have a component of several or all of these. Right v. Left Ventricular Pump Failure Lf Heart Failure Case Study • • • • • • • ID/CC. 56 year old female with COPD presents to the ER with extreme dyspnea at rest. HPI. Increasing productive cough and exertional dyspnea. 80 pack year hx of cigarette smoking. Currently 3 pack/day despite sypmt and dx of COPD. PE. JVD with large a and v waves, cyanosis, labored breathing, ankle and sacral edema, tender hepatomegaly. Labs. ECG= rt axis deviation, peaked p waves. Pulmonary function tests = COPD pattern. CXR. Rt ventricular and PA enlargement. Rt heart catheterization. Pulmonary hypertension. Gross Anatomy. Right ventricular hypertrophy. Summary •The relationship of ventricular pressures and volumes determines CO. RV peak systolic pressure is 4 to 5 x less than the LV. –During systole the RV pumps like a bellows . –The LV contracts from apex to base with a counter-clockwise twist. •Systolic durations are ~ equal; isovolumetric phase of PV loops represent the longer time required to reach the and match aortic verses pulmonic arterial diastolic pressure (afterload). –Greater LV pressure alter phasic wave while the volumes moved are approximately equal with LV/RV volume mismatches continuously being resolved. Summary • Ventricles with increased contractility operate at a lower enddiastolic volume/ pressure and achieve end-systolic pressure at a lower end-systolic volume. – In contrast, ventricles with impaired contractility operate at a high enddiastolic volume and pressure and achieve end-systolic pressure at higher end-systolic volumes. • The slope of a line from the origin through the end-systolic pressure point is measures the contractile state. – PV loops with end-systolic points on the same line are generated when loading conditions are changed, but contractility is unaltered. – This measure of contractility is relatively load-independent. Summary • PV Loops are modulated by both intrinsic and extrinsic phenomena. • Increased contractility, an intrinsic cardiac property increases contractility and decreases LV end systolic volume (ESV). – If the systemic pressure is unaltered then the systemic circulation receives this increased stroke volume (SV). – Extrinsic factors like increased preload increases LV end diastolic volume (EDV) but do not alter LVESV and SV increases. Summary • As pump flow varies cardiac output changes central venous pressure (CVP) and right atrial pressure (RAP). – RAP responds to increasing venous return that must be matched by an increase in cardiac function. – That is, ventricular function must increase to increase output and bring venous return to equilibrium. – For example, increasing blood volume shifts the vascular function curve to the right (Return to RA) and the match between the cardiac output and venous return now occurs at a higher RAP. Summary • In normally compliant myocardium, contractility is the intrinsic function that alters the end systolic pressure volume relationships. – Expressed as the maximal rate of pressure change per time change, maximum “dp/dt” or dpdtmax is the velocity measured during isovolumetric contraction. – It is the most accurate measure of in vivo ventricular systolic performance and independent of afterload. – Cardiac catheterization is required to determine this performance parameter. • Heart failure is the inability of the heart to pump sufficient blood to maintain normal exercise. – The greater the failure the lesser the cardiac reserve. – Clinically, cardiac reserve can be approximated by determining cardiac output power at rest and at VO2 max.